Muaj peev xwm kho tau cov txiaj ntsig ntawm Natural Plant Compounds hauv raum Kab Mob

Emailtina.xiang@wecistanche.comkom paub meej ntxiv.

Paub meej: Keeb kwm: Qhov thaiv ntawm qhov kev loj hlob lossis qhov pib ntawm cov xwm txheej pathological yog qhov tseem ceeb rau kev ua haujlwm ntawm lub cev. Qee cov txheej txheem pathological uas cuam tshuam nrog ntau yam kab mob yog cov tswj tsis taumobCov tshuaj tiv thaiv uas txhawb nqa fibrosis, oxidative tshua, thiab lwm yam kev hloov pauv. Ntuj cog tebchaw (NPCs) yog cov khoom siv bioactive tau los ntawm cov khoom ntuj tsim uas tuaj yeem tswj cov txheej txheem physiological. Kev mob tshwm sim tau lees paub tias yog ib qho tseem ceeb hauv kev txhim kho thiab kev hloov pauv ntawm lub raum tsis zoo. Yog li ntawd, txhua qhov sib xyaw ua ke tuaj yeem hloov kho qhov mob lossis cov txheej txheem o tuaj yeem xav tias yog tus neeg saib xyuas lub raum thiab / lossis cov cuab yeej kho mob uas muaj peev xwm tswj tau lub raum puas. Lub hom phiaj ntawm qhov kev tshawb fawb no yog los tshuaj xyuas cov txiaj ntsig zoo ntawm bioactive natural compounds ntawmraumkev puas tsuajqhia lawv cov kev ua tau zoo raws li tau pom hauv kev tshawb fawb soj ntsuam. Cov Txheej Txheem: Qhov kev tshuaj xyuas zoo no yog ua raws li cov kev tshawb fawb ntsig txog kev cuam tshuam ntawm NPCs nrog cov peev txheej kho mob rauraumkab mobkev kho mob hauv tib neeg. Cov txiaj ntsig: Cov kev tshawb fawb soj ntsuam tau soj ntsuam NPCs raws li txoj hauv kev sib txawv los kho lossis tiv thaiv lub raum puas thiab tshwm sim los qhia qee qhov txiaj ntsig hauv kev txhim kho OS, o, thiab muaj peev xwm antioxidant, yog li ua rau lawv cog lus cov cuab yeej kho mob kom txo lossis tiv thaiv qhov pib thiab kev loj hlob ntawm KD pathogenesis. . Cov ntsiab lus xaus: Qhov kev tshuaj xyuas no qhia tau hais tias qhov chaw kho mob tau zoo ntawm NPC hauv KD txoj kev kho. Txawm li cas los xij, yuav tsum muaj kev sim tshuaj muaj zog ntau dua los tsim kom muaj kev nyab xeeb thiab kho cov teebmeem hauv thaj tsam ntawm lub raum puas.

Ntsiab lus: ntuj cog tebchaw; kab mob raum; cov teebmeem renoprotective; bioactive compounds; kev tshawb fawb soj ntsuam

1. Taw qhia

Keeb kwm, natural plant compounds (NPCs) tau siv los ua kev kho mob thiab lawv cov qauv tshuaj tuaj yeem ua rau muaj kev xaiv kho tshiab [1]. NPCs yog cov tshuaj nquag cais tawm los ntawm cov nroj tsuag uas tuaj yeem hloov kho ntau txoj hauv kev, suav nrog kev hloov pauv ntawm epithelial-to-mesenchymal (EMT) ntawm cov tshuaj antioxidant,anti-inflammatory, los yog anti-fibrotic mechanisms [1]. Ntevraumkab mob(CKD) yog ib qho teeb meem kev noj qab haus huv thoob ntiaj teb rov tshwm sim [2]. Ntau yam kab mob (piv txwv li, ntshav siab, ntshav qab zib mellitus, mob qog noj ntshav, mob qog noj ntshav, mob nephrotoxicity) tuaj yeem cuam tshuam.raummuaj nuj nqi, nws thiaj li ua rau CKD txoj kev loj hlob. Nyob ib ncig ntawm lub ntiaj teb no, qhov tshwm sim ntawm CKD yog 13.4 feem pua ​​(11.7–15.1 feem pua) thiab nws tau kwv yees tias cov neeg mob uas muaj kab mob raum kawg (ESRD), uas yuav tsum tau kho raum pauv, tus lej ntawm 4.902 thiab 7.083 lab, ua rau nws. ib qho ua rau tuag thoob ntiaj teb [2,3]. Cov neeg mob CKD ntau dua nyob rau xyoo tas los no tau ua rau muaj kev txaus siab rau kev tshawb nrhiav kom tau txais txiaj ntsig zoo kom zam lossis txo qhov kev loj hlob ntawm CKD thiab nws txoj kev loj hlob mus rau ESRD. Kev kho mob ib txwm muaj kev tiv thaiv rau lub raum tsawg, yog li cov tshuaj kho tshiab yog tsim nyog. Tam sim no, qhov mob tau lees paub tias yog txoj hauv kev tsis zoo hauv txoj kev loj hlob thiab kev loj hlob ntawm CKD; yog li ntawd, tshiabanti-inflammatoryCov tshuaj tiv thaiv los yog qhia rau cov cim tshwj xeeb molecular tej zaum yuav muaj kev cog lus kho mob rau CKD. NPCs muab tau los ntawm cov tshuaj ntsuab lossis cov nroj tsuag tshuaj tau dhau los ua qhov tseem ceeb hauv kev tshawb fawb txog kev kho mob thiab kev kho mob rau kev txhim kho cov hom phiaj. Ob peb NPCs tau pom tias muaj cov nyhuv renoprotective thiab txhim kho cov txiaj ntsig ntawm cov teeb meem tshwm sim hauv ntau pawg ntawm CKD hauv kev tshawb fawb soj ntsuam, feem ntau los ntawm kev ua kom muaj zog tiv thaiv kab mob antioxidant thiab txo qis.pro-inflammatory cov kev taw qhia (Table 1; Daim duab 1)[3]. Qhov kev tshuaj xyuas no tau sau cov ntaub ntawv pov thawj ntawm lub raum-tiv thaiv muaj peev xwm ntawm bioactive nroj tsuag tebchaw.

2. Cov txheej txheem

Qhov kev tshuaj xyuas no yog ua raws li cov ntaub ntawv tsim nyog tau tshaj tawm los ntawm kev xaiv tshawb fawb siv cov ntsiab lus tseem ceeb uas tau sau los ntawm cov ntaub ntawv xws li Science Direct, EBSCO, Scopus, thiab PubMed txhawm rau txheeb xyuas cov kev sim tshuaj ntsuam xyuas qhov muaj feem cuam tshuam ntawm natural bioactive compounds txog lawv cov kev kho mob zoo li. kev kho mob raum kab mob. Lub hom phiaj tseem ceeb ntawm qhov kev tshuaj xyuas no ntawm cov teebmeem ntawm bioactive natural compounds rauraum kev puas tsuajyog los nthuav qhia cov kev ua tau zoo uas tau pom hauv kev tshawb fawb soj ntsuam.

3. Cov txiaj ntsig

3.1.Molecular Mechanisms cuam tshuam rau lub raum puas

Lub raumkev puas tsuajyog ib qho teeb meem kev noj qab haus huv thoob ntiaj teb uas tau loj hlob thoob ntiaj teb. Cov kab mob raum muaj mob hnyavrauminjury(AK) and CKD, which can lead to ESRD. Consequently, patients needing renal replacement therapy are estimated to number between 4.902 and 7.083 million [2,3]. The worldwide projected prevalence of CKD is 13.4%(11.7-15.1%)[2]; likewise, in 2017, the global prevalence of CKD was 9.1%, ie., approximately 700 million cases [29]. CKD is frequently asymptomatic with fast progression and is commonly associated with hypertension [30] and Type 2 diabetes mellitus (T2DM). These diseases are considered the leading causes of the development of CKD and ESRD [31]. Nevertheless, CKD is a chronic disorder characterized by albuminuria (>30 mg) rau 24 teev, txo glomerular filtration rate (GFR) (<60 ml/min/1.73="" m)="" for="" more="" than3="" months,="" and="" progressive="" glomerular,="" tubular,="" and="" interstitial="" damage="" [32-34].="" the="" prognosis="" of="" ckd="" is="" classified="" according="" to="" the="" gfr="" and="" albuminuria="" categories,="" gf="" grades(g1="" to="" g5),="" and="" albuminuria="" grades(a1="" to="" a3)(figure="" 2),="" according="" to="" the="" kidney="" disease:="" improving="" global="" outcomes="" guidelines="" (kdigo="" 2012),="">

Pawg yog pawg los ntawm kev pheej hmoo ntawm kev nce qib, txhais los ntawm kev poob qis hauv qeb GFR. Hloov los ntawmLub raumKab mob: Txhim kho Cov txiaj ntsig thoob ntiaj teb (KDIGO 2012) pawg ntawm Lub TebchawsLub raumFoundation (NFK). ESKD, kab mob raum kawg; CVD, kab mob plawv; CKD, mob raum mob; GFR, glomerular pom tus nqi. Qee cov ntsiab lus ntawm daim duab no tau raug coj los ntawm Lub Siab Cov Duab Platform, muaj nyob ntawm www.mindthegraph.com. (Hnub kawg ntawm kev nkag; 30 Cuaj hlis 2021).

Muaj ntau txoj hauv kev qhia txog kev qhia txog molecular yog cuam tshuam rau qhov pib thiab kev loj hlob ntawm lub raum puas, suav nrog renin-angiotensin system (RAS), uas yog lub hauv paus tswj hwm ntawmraumfibrosis. Ua ke, cov ntaub so ntswg thiab cov hlab ntsha RAS ntseeg tau tias yog overstimulated nyob rau hauv kev kawm ntawmraumstimulation ntawm fibrosis. RAS nce qib ntawm angiotensin II (Ang II), uas ua lub luag haujlwm tseem ceeb hauv lub raum fibrosis los ntawm kev kho kom muaj kev ywj pheej ntawm kev hloov pauv kev loj hlob (TGF-) thiab pib.mobtxheej txheem [36–39]. Ib yam li ntawd, Ang II thiab o tuaj yeem yog qhov tseem ceeb hauv cov kab mob glomerulotubular cov lus teb thiab tau cuam tshuam nrog microalbuminuria thiab kev loj hlob ntawm cov kab mob.raumkev puas tsuaj[40]. Hauv cov neeg mob ntshav qab zib mellitus thiab hyperglycemia hnyav, ntau qhov kev cuam tshuam ntawm metabolic thiab hemodynamic tshwm sim, suav nrog kev nce qib ntawm cov khoom siv glycation kawg (AGEs), augmented reactive oxygen hom (ROS) tiam, thiab pib ntawm cov protein kinase C (PKC) thiab polyol. txoj hauv kev, uas ntseeg tau tias yuav txhawb kev txhim kho thiab hloov pauv ntawm cov ntshav qab zib nephropathy [39]. Lwm txoj hauv kev molecular uas ua rau lub raum puas tsuaj yog tsim ntawm AGEs, uas txhawb nqa cov kab mob hauv lub cev nitric oxide (NO) thiab ROS, thiab mitogen-activated protein kinase (MAPK) cascade. Kev tsim ntawm AGEs tuaj yeem ua rau lub raum puas tsuaj los ntawm kev hloov pauv lub luag haujlwm ntawm cov proteins, oxidative stress (OS), pro-inflammatory cytokines, thiab kev loj hlob [41-43]. Tsis tas li ntawd, AGE-RAGE kev sib cuam tshuam induces activation ntawm nuclear factor kappa-light-chain-enhancer ntawm triggered B hlwb (NF-kB) thiab ua kom MEK thiab MAP kinases, nce intracellular OS los ntawm stimulating NADPH oxidase, ib tug tseem ceeb regulator nyob rau hauv superoxide radical tiam [44,45]. Ib yam li ntawd, ROS thiab dawb radicals tuaj yeem teb rau daim nyias nyias lipids, nucleic acids, thiab cov proteins, thiab pib tsim cov cellular raug mob. Thaum ROS raug tsim nyob rau hauv ntau ntau, OS, antioxidant tiv thaiv mechanisms thiab cell puas tuaj yeem tshwm sim, uas ua rau kev nce qib ntawm CKD. Lwm txoj hauv kev cuam tshuam nrog CKD pathogenesis yog kev ntxhov siab stimuli thiab ua kom muaj kev loj hlob ntawm profibrotic xws li TGF- 1, txuas cov nqaij mos loj hlob (CTGF), thiab hydrogen peroxide (H2O2). Tsis tas li ntawd, TGF- tau pom tias yuav nce ROS ntau lawm thiab txo cov kab mob antioxidant, yog li inducing OS thiab / lossis redox tsis txaus. Qhov tseem ceeb, redox imbalance tseem ceeb pab TGF-'s pathophysiologic zog xws li fibrosis [46,47]. TGF- tuaj yeem tsav mus rau lub raum fibrosis los ntawm kev sib sau ntawm extracellular matrix (ECM) thiab ua kom cov epithelial dysfunction thiab pro-mobcov tshuaj tiv thaiv. TGF- yog lub zog muaj zog tshaj plaws ntawm EMT, thiab qhov no tuaj yeem ua rau cov txheej txheem no nyob rau hauv cov hlwb epithelial ntawm ntau yam kabmob hauv vivo thiab hauv vitro [48–51]. Kev taw qhia txoj hauv kev xws li MAPK, Smad, thiab PI3K txoj hauv kev muaj feem xyuam nrog kev txhawb nqa ntawm EMT los ntawm TGF- [52,53]. Qhov tseem ceeb, ROS los ntawm ntau qhov chaw, xws li mitochondria lossis NOXs, uas tau raug TGF- - ntxias EMT thaum pib ntawm fibrosis thiab mob qog noj ntshav [49,50,54–56]. Cov pov thawj tsis ntev los no tau qhia txog cov txheej txheem ntawm kev txuas ROS rau TGF- - qhib EMT hauv cov ntsiab lus ntawm fibrosis [48,49,57]. Rhyu et al. tshawb pom tias NADPH oxidase-originated ROS yog cov khoom siv hluav taws xob tshaj tawm hauv TGF- 1-stimulated fibronectin thiab tsim cov plasminogen activator inhibitor-1 (PAI-1). Cov kauj ruam no tshwm sim thoob plaws MAPK stimulation hauv tubular epithelial hlwb [57]. Ib yam li ntawd, lwm cov kev tshawb fawb tau qhia tias ROS ua lub luag haujlwm tseem ceeb hauv TGF- 1- qhib EMT, feem ntau los ntawm MAPK stimulation [58,59]. Cov txheej txheem no sib tshooj thiab sib cuam tshuam nrog ib leeg, yog li hloov kho lawv cov dej num lom neeg, uas txhawb kev hloov pauv ntawm lub raum fibrosis thiab exacerbates raum.kev puas tsuaj(Daim duab 3). Yog li ntawd, txhua tus kws kho mob uas muaj peev xwm tiv thaiv txoj hauv kev tsis zoo no tuaj yeem xav tias yog renoprotective thiab muaj peev xwm kho tau hauv kev tswj lub raum.kev puas tsuaj.

3.2.Potential Renoprotectize los ntawm qee cov nroj tsuag ntuj

3.2.1.Allicin (DiallylThiosulfinate)

Lub ntsiab bioactive cov khoom ntawm qej (Allium satioum L.) yog organosulfur compounds (OSCs). Ntawm cov tebchaw no, feem ntau cov sulfur sib xyaw uas muaj nyob rau hauv cov qij tshiab thiab qhuav yog allin (S-allyl-I-cysteine ​​sulfoxide) [60,61]. Allin tuaj yeem hloov pauv sai sai rau hauv allicin (diallyl thiosulfinate) [61], uas tau piav qhia tias yog QSC loj thiab tau tshaj tawm tias yog ib qho ntawm cov khoom tseem ceeb ntawm cov tshuaj tiv thaiv kab mob (33), immunomodulatory, anti-inflammatory [62], antioxidant [63], thiab lwm yam pharmacological zog [61]. Alliin kuj muaj cov khoom tsis yog sulfur uas tej zaum yuav muaj kev sib koom ua ke lossis cov khoom ntxiv nrog OSCs [64].

Ib qho kev tshawb nrhiav ob qhov muag tsis pom kev soj ntsuam kev tshawb fawb soj ntsuam cov txiaj ntsig ntawm qej extract ntawm cov ntshav.mobCov cim ntawm 42 cov neeg mob uas raug mob peritoneal dialysis (PD), kev kho lub raum tsis ua haujlwm. Cov neeg mob tau txais ib koob tshuaj ntawm 400 mg ntawm cov qauv qej extract, uas tau ua nyob rau hauv cov duab ntawm cov ntsiav tshuaj nrog rau 1 mg (1000 mcg) ntawm alliin. Txoj kev siv tshuaj nyob rau hauv pawg neeg mob (qej extract pawg) yog ob zaug hauv ib hnub rau 8 lub lis piam, thaum pawg tswj hwm tau txais cov qauv kev kho mob ntxiv rau cov placebo nyob rau tib lub sijhawm. Cov txiaj ntsig tau pom tias nyob rau hauv cov neeg mob uas tau txais cov qej extract, cov cim inflammatory IL-6, C reactive protein (CRP), thiab erythrocyte sedimentation rate (ESR) tau tag nrho txo ​​qis, thaum nyob rau hauv cov placebo pab pawg, a Kev txo qis tseem ceeb tsuas yog pom hauv IL-6. Txawm li cas los xij, kev ntsuam xyuas ntawm cov teebmeem no hauv kev sim loj dua tau pom zoo [4].

3.2.2. Astaxanthin

Xanthophyll carotenoid colourant muaj cov txiaj ntsig zoo, suav nrog tshuaj tua kab mob, tshuaj tua kab mob, thiab tshuaj tiv thaiv kab mob. Feem ntau ntawm astaxanthin (AST; 3, 30 -dihydroxy- , '-carotene-4, 40 -dione) raws li siv hauv cov khoom noj khoom haus yog tau los ntawm Haematococcus alga [65]. Lub Chaw Tswj Xyuas Khoom Noj thiab Tshuaj (FDA) ntawm Tebchaws Meskas tau lees txais astaxanthin ua nutraceutical [66]. Kev tshawb fawb hauv tib neeg tau pom qhov txo qis hauv OS, dyslipidemia, thiabmobCov cim tom qab kev tswj qhov ncauj ntawm astaxanthin. Kev soj ntsuam kuaj mob plabmobbiomarkers tau ua nyob rau hauv cov neeg mob uas muaj kev ua haujlwm dyspepsia kho nrog astaxanthin thiab qhia tias muaj kev nce ntxiv hauv CD4 ntxiv rau cov hlwb thiab txo qis hauv CD8 ntxiv rau T hlwb hauv 21 cov neeg mob uas muaj Helicobacter pylori (H. pylori) kho nrog 40 mg ntawm astaxanthin txhua hnub thiab 23 tus neeg mob. muab cov placebo, yog li cov kws sau ntawv tau hais tias qhov sib txawv no qhia tau tias muaj kev hloov pauv ntau dua rau kev tiv thaiv kab mob humoral tsis yog cov lus teb cytotoxic [67]. Ntxiv mus, lawv tau piav qhia tias hauv cov qauv tsiaj, qhov twg cov khoom noj tuaj yeem ua qauv tsis muaj tshuaj tua kab mob, astaxanthin muaj txiaj ntsig zoo rau kev mob thiab ntawm qhov ntom ntawm H. pylori [68].
Ib yam li ntawd, kev sim tshuaj placebo-tswj randomized tau ua los tshawb xyuas qhov ua tau ntawm kev tswj hwm ntawm astaxanthin ntawm lipid peroxidation, qib adiponectin, glycemic tswj, anthropometric indices, thiab insulin rhiab heev rau cov neeg mob nrog T2DM, uas yog ib qho ua rau thiab ua rau lub raum.kev puas tsuaj. Hauv pawg kev tshawb fawb, tom qab 8 lub lis piam ntawm 8 mg ntawm astaxanthin kev tswj hwm, cov ntshav adiponectin concentration tau nce ntxiv thiab muaj qhov txo qis hauv lub cev rog rog (p < 0.01),="" ntshav="" triglycerides,="" tsawg-density.="" lipoprotein="" cholesterol="" (vldl-c),="" qib="" systolic="" ntshav="" siab="" [5].="" cov="" neeg="" tshawb="" xyuas="" tau="" qhia="" tias="" astaxanthin="" tuaj="" yeem="" muab="" cov="" txiaj="" ntsig="" zoo="" ntawm="" cov="" hlab="" ntsha="" thiab="" txo="" qhov="" ntsuas="" ntawm="" os="" thiab="" o="" [69];="" txawm="" li="" cas="" los="" xij,="" lawv="" cov="" txiaj="" ntsig="" tau="" pom="" tias="" 12="" mg="" ntawm="" qhov="" ncauj="" astaxanthin="" hnub="" rau="" 12="" lub="" hlis="" tsis="" muaj="" txiaj="" ntsig="" zoo="" rau="" cov="" hlab="" ntsha,="" os,="" lossis="" mob="" raum="" rau="" cov="" neeg="" tau="" txais="" kev="" hloov="" pauv="" [70].="" txawm="" li="" cas="" los="" xij,="" nws="" tau="" raug="" pov="" thawj="" hauv="" cov="" qauv="" tsiaj="" uas="" astaxanthin="" muaj="" kev="" tiv="" thaiv="" rau="" lub="" raum="" kev="" puas="" tsuaj="" los="" ntawm="" kev="" tswj="" kev="" mob="" (inducing="" cd8="" ntxiv="" rau="" t="" hlwb)="" [71]="" thiab="" oxidative="" stress-related="" nrf2/keap1="" and="" ros="" pathways="" [72].="" yog="" li,="" txawm="" hais="" tias="" astaxanthin="" tau="" ua="" kom="" pom="" cov="" tshuaj="" tiv="" thaiv="" antioxidant,="" tiv="" thaiv="" kab="" mob,="" thiab="" vascular="" tiv="" thaiv="" los="" ntawm="" cov="" kab="" mob="" sib="" txawv,="" ntau="" cov="" kev="" tshawb="" fawb="" yuav="" nthuav="" qhia="" nws="" lub="" peev="" xwm="" los="" txhim="" kho="" ckd="" pathogenesis="" hauv="" tib="">

3.2.3. Baicalin

Nws yog flavone glycoside cais los ntawm cov hauv paus hniav ntawm Scutellaria baicalensis. Cov kev tshawb fawb soj ntsuam nrog baicalin raws li kev kho mob ntxiv tau tsom rau kev tiv thaiv kev ua haujlwm hauv daim siab fibrosis, ulcerative colitis, thiab ntshav qab zib mellitus [73,74]. Ntau cov kev tshawb fawb tau tshawb fawb txog qhov muaj peev xwm ntawm baicalin hauv kev tswj cov kev kawm nrog rau mob ntshav qab zib thaum ntxov [75]. Cov txiaj ntsig ntawm baicalin tau txheeb xyuas hauv cov neeg mob ntshav qab zib nephropathy ntawm koob tshuaj 800 mg peb zaug hauv ib hnub, thaum pawg tswj hwm tau txais cov placebo. Ob pawg tau kho

thiab kawm tau 6 lub hlis. Cov txiaj ntsig tau qhia tias baicalin muaj peev xwm txo qis qib ntawm cov proteinuria thiab txhim kho lub raum ua haujlwm ntawm cov neeg mob ntshav qab zib vim tias tom qab noj baicalin kho, superoxide dismutase (SOD) thiab glutathione peroxidase (GSH-px) cov neeg mob tau pom meej meej, thiab cov kev ua ntawm aldose reductase (AR), NF-κB, thiab vascular endothelial kev loj hlob yam (VEGF) cov ntsiab lus txo qis heev. Cov txiaj ntsig no tau pom tias baicalin ntawm koob tshuaj 800 mg peb zaug hauv ib hnub tuaj yeem txo lub raum vascular permeability, txhim kho lub raum kev ua haujlwm ntawm cov neeg mob ntshav qab zib nephropathy, thiab ncua kev nce qib ntawm cov ntshav qab zib nephropathy ntawm txoj hauv kev polyol, thiab cov tshuaj tiv thaiv kev ntxhov siab, tiv thaiv. inflammatory, thiab lwm yam. Cov kev tshawb fawb ntxiv yog xav tau los ntsuam xyuas cov teebmeem nephroprotective ntawm baicalin los ntawm lwm cov txheej txheem [8].

Kev tshawb fawb soj ntsuam txhawm rau ntsuas qhov kev ua ntawm baicalin ntawm AKI hauv menyuam yaus sepsis. Qhov kev tshawb fawb soj ntsuam no suav nrog 50 tus neeg mob menyuam yaus uas kuaj pom tus mob sepsis, 25 tus neeg tau txais kev kho mob ntawm qhov ncauj baicalin rau 15 hnub thiab lwm tus neeg mob 25 tau txais kev kho mob nkaus xwb. Lawv cov txiaj ntsig tau pom tias tsis yog cov ntshav urea nitrogen (BUN) lossis cov ntshav creatinine concentrations ntawm pawg tswj hwm tau hloov pauv ntau tom qab kev kho mob yooj yim, tab sis lawv tau txo qis hauv baicalin adjunctive therapy group. Nws tuaj yeem xav tias, raws li ob qhov ntsuas no, tias lub raum ua haujlwm ntawm pab pawg baicalin txhim kho, tej zaum vim yog kev kho baicalin adjunctive. Yog li ntawd, baicalin tuaj yeem txo AKI hauv cov neeg mob sepsis. Txawm hais tias txoj kev tshawb fawb no tau qhia txog kev tiv thaiv ntawm baicalin tiv thaiv AKI hauv pawg kev tshawb fawb no, pom tias yog qhov txo qis hauv BUN thiab creatinine qib, cov kws sau ntawv tsis tau tshaj tawm cov tshuaj noj thiab yog li qhov tsim nyog ntau npaum li cas thiab cov teeb meem tshwm sim yuav tsum tau soj ntsuam hauv cov kev tshawb fawb tom ntej [ 76] ib.

3.2.4. Betalain

Lwm NPC nrog cov khoom nthuav hauv lub raum kab mob yog betalain. Betalains tau muab faib ua ob pawg: Betacyanins, uas tsim cov xim liab thiab yog tsim los ntawm condensation ntawm ib tug cyclo-DOPA (dihydroxyphenylalanine) qauv nrog betalamic acid, thiab betaxanthines, uas tsim daj xim thiab yog synthesized los ntawm txawv amino compounds thiab betalamic acid [77] ]. Ib qho kev sim hla kev soj ntsuam kuaj xyuas seb puas noj zaub mov ntawm betalain-nplua nuj extract los ntawm liab beetroot thiab ib tug betacyanin-nplua nuj extract ntawm Opuntia stricta txiv hmab txiv ntoo muaj peev xwm los hloov cov noob / protein qhia nyob rau hauv cov kab mob coronary artery (CAD) cov neeg mob. CKD yog ib qho kev pheej hmoo loj rau CAD. Cov neeg mob uas muaj CKD pom tias muaj kev kub ntxhov siab heev, thiab kab mob plawv (CVD) yog qhov ua rau mob hnyav thiab tuag rau cov neeg mob no. Qhov muaj feem ntau ntawm cov kab mob CAD ib txwm muaj, xws li ntshav qab zib thiab kub siab, txhais tau hais tias cov neeg mob no kuj raug rau lwm yam uas tsis yog cov kab mob uremia ntsig txog CVD, suav nrog o, oxidative kev nyuaj siab, thiab txawv txav calcium-phosphorus metabolism [78].

Nyob rau hauv ib tug randomized crossover sim, 48 txiv neej coronary artery kab mob cov neeg mob tau txais txog 50 mg ntawm betalain los yog betacyanin txhua hnub rau 2 lub lis piam nyob rau hauv peb lub sij hawm sib cais los ntawm lub sij hawm ntxuav tawm. Cov neeg mob tau muab faib ua peb pawg nyob ntawm qhov ntxiv: betalain-nplua nuj ntxiv ntawm liab beetroot (Beta vulgaris), Betacyanin-nplua nuj ntxiv ntawm prickly pear cactus (Opuntia stricta), thiab cov placebo. Cov txiaj ntsig tau pom tias betalain nce sirtuin-1 (SIRT1) thiab txo qis lectin zoo li oxidized LDL receptor 1 (LOX1) thiab C reactive protein ntau (hs-CRP) hauv cov ntshav peripheral mononuclear hlwb (PBMCs) ntawm cov neeg mob. Cov txiaj ntsig no yuav yog vim qhov txo qis hauv OS thiab o ntawm cov tshuaj tiv thaiv antioxidant thiab tiv thaiv kab mob ntawm betalains. Yog li, betalains tuaj yeem cog lus lwm txoj hauv kev rau kev kho mob ntxiv hauv OS, o, thiab cov kab mob kev laus. Txawm li cas los xij, kev tshuaj xyuas ntxiv yog tsim nyog kom nkag siab tob txog lawv cov haujlwm tshwj xeeb ntawm lub cev [9,79,80].

3.2.5. Beetroot Kua txiv

Nws yog ib qhov chaw ntawm concentrated inorganic nitrates. Ib txoj kev tshawb fawb txog cov neeg mob CKD (CKDSstage II-IV raws li K/DOQI (Kidney Outcomes Quality Initiative) cov lus qhia) los ntawm Kemmner li al. qhia tias kev tswj hwm ntawm cov kua txiv beetroot nrog ib qho nitrate load ntawm 300 mg rau cuaj tus neeg mob tau nce nitric oxide (NO) concentrations thiab txo qis rau lub raum index (RRI), uas yog cov cim qhia txog kev mob plawv, piv nrog cov placebo [10]. Qhov txiaj ntsig no tau tshwm sim ntau dua ntawm cov neeg mob CKD uas muaj lub raum tsis ua haujlwm thiab nce cov hlab ntsha, uas muaj GFR qhov tseem ceeb qis dua qhov qub. Qhov kev txo qis no feem ntau yog tshwm sim los ntawm kev mob ntshav qab zib lossis mob raum tsis ua haujlwm, ob qho tib si yog qhov tseem ceeb rau qhov tshwm sim tom qab ntawm lub raum tsis ua haujlwm. Piv nrog rau kev tswj hwm, cov ntshav creatinine, potassium, thiab GFR cov ntshav tsis tau hloov pauv ntau tom qab noj cov kua txiv beetroot. Cov piam thaj hauv ntshav concentration / qib zoo ib yam li cov placebo pawg. Cov txiaj ntsig tau tsim qhov kev txhim kho ntawm Beta vulgaris yog qhov kev xaiv kho tau zoo ntawm cov cim ntawm lub raum kev ua haujlwm, txo qis qis qis ntawm lub raum kev puas tsuaj thiab kev tuag tom qab hauv cov pab pawg muaj kev pheej hmoo siab nrog rau cov neeg mob ntshav siab thiab mob ntshav qab zib nephropathy [10].

3.2.6. Berberine (BBR)

Nws yog ib qho isoquinoline alkaloid thiab yog lub ntsiab active compound cais los ntawm Rhizoma coptidis thiab Cortex Phellodendron. Cov kev tshuaj ntsuam tshiab tau pom tias berberine muaj ntau cov txiaj ntsig tshuaj, xws li txo cov ntshav qabzib, ua haujlwm antioxidant, tswj cov ntshav lipid, txo qhov mob, thiab nce cov tshuaj insulin, yog li txhim kho insulin tsis kam [81,82]. Tsis ntev los no, nws tau raug piav qhia tias muaj peev xwm tiv thaiv ntshav qab zib nephropathy tshuaj [83]. Cov zis microalbumin / creatinine piv (UACR) thiab GFR yog cov cim tseem ceeb uas siv los ntsuas qhov xwm txheej ntawm ntshav qab zib nephropathy. Qhov kev sim tshuaj ntsuam xyuas randomized tau ua los saib cov teebmeem ntawm berberine cuam tshuam rau cov ntshav Cys C thiab UACR hauv cov neeg mob T2DM. Cov kws tshawb fawb tau tswj hwm berberine ntawm ib koob ntawm 0.4 g peb zaug hauv ib hnub rau 6 lub hlis. Lawv cov txiaj ntsig tau pom tias berberine txhim kho cov kab mob hauv lub raum los ntawm kev txo UACR thiab cov ntshav Cys C hauv cov neeg mob T2DM, thiab cov txiaj ntsig tau muaj txiaj ntsig zoo. Txawm li cas los xij, cov kws sau ntawv tau hais tias muaj pes tsawg tus neeg mob hauv lawv txoj kev kawm tsawg thiab lub sijhawm soj ntsuam tsis ntev txaus, yog li nws yog qhov tseem ceeb los txheeb xyuas qhov ua tau zoo thiab kev nyab xeeb ntawm berberine hauv kev nce qib ntawm CKD [11]. Berberine tau pom tias tiv thaiv lub raum tubular hlwb tiv thaiv hypoxia / reoxygenation raug mob ntawm Sirt1 [84].

3.2.7 ib. Cordycepin

Nws yog ib txwm muab los ntawm cov khoom sib xyaw ua ke uas tsim los ntawm Cordyceps militaris, teej tug mus rau tsev neeg Clavicipitaceae. Nws yog cov kab mob fungus uas muaj keeb kwm ntev ntawm kev siv tshuaj ib txwm siv thiab nws cov ntsiab lus tshwj xeeb, cordycepin, muaj ntau yam kev txhawb nqa kev noj qab haus huv, suav nrog tshuaj tiv thaiv kab mob, tiv thaiv kab mob, tiv thaiv kab mob, tshuaj tiv thaiv kab mob, thiab tshuaj tiv thaiv kab mob [85-87]. Tsis tas li ntawd, cov tshuaj tiv thaiv kab mob ntshav qab zib thiab nephroprotective tau raug ntaus nqi rau cordycepin hauv kev tshawb fawb sim [88]. Hauv kev tshawb fawb soj ntsuam nrog cov neeg mob CKD, Cordyceps militaris tau noj 100 mg txhua hnub thiab piv nrog cov placebo (tswj pab pawg). Cordyceps militaris txo cov protein ntau ntawm TLR4, NF-κB p65, COX2, IL-1 , thiab TNF- . Lawv cov txiaj ntsig tau pom tias eGFR tau txais txiaj ntsig zoo dua piv nrog pawg tswj hwm tom qab 3 lub hlis ntawm kev kho mob. Qhov no tau qhia tias Cordyceps militaris tau txhim kho eGFR ntawm cov neeg mob CKD, thiab cov txiaj ntsig tau pom tias Cordyceps militaris ameliorated raum ua haujlwm thiab tswj cov ntshav hauv zis, BUN, thiab creatinine. Txoj kev tshawb no tau muab kev txhawb nqa rau qhov ua tau tias Cordyceps militaris tswj CKD evolution los ntawm kev tswj TLR4 / NF-κB redox signaling txoj kev [12].

3.2.8 ib. Curcumin

Nws yog ib feem ntawm turmeric (Curcuma longa). Curcumin (diferuloylmethane) tau pom tias yog TNF blocker hauv vitro thiab hauv vivo; Txawm li cas los xij, tsuas yog qee qhov kev soj ntsuam tsawg tau lees paub tias curcumin muaj txiaj ntsig ntawm kev txo TGF- , IL-8, thiab TNF- qib hauv preclinical [89] thiab kev tshawb fawb soj ntsuam [90]. Muaj ntau ntau qhov ua rau muaj kev cuam tshuam rau cov kab mob ntshav qab zib lub raum puas tsuaj, tab sis TGF- raug suav tias yog ib qho tseem ceeb hauv kev ua haujlwm ntawm ESRD. Hauv kev tshawb fawb randomized ob qhov muag tsis pom kev placebo-tswj, cov teebmeem ntawm turmeric ntawm TGF- , IL-8, thiab TNF- qib, nrog rau cov proteinuria hauv cov zis thiab ntshav, tau tshawb xyuas hauv cov neeg mob T2DM nephropathy (n.=20) thiab pawg tswj hwm (n=20). Ib leeg, pawg neeg xeem tau muab ib lub tshuaj ntsiav uas muaj 500 mg turmeric, 22.1 mg ntawm cov uas yog cov tshuaj curcumin, muab rau txhua pluas noj (peb tsiav tshuaj txhua hnub) rau 2 lub hlis. Lawv cov txiaj ntsig tau pom tias cov ntshav qab zib TGF- thiab IL-8 qhov tseem ceeb tau qis qis dua tom qab kev tswj hwm ntawm turmeric thiab tias cov turmeric supplementation luv luv tuaj yeem txo cov proteinuria. Tsis tas li ntawd, lawv tsis tau tshaj tawm txog qhov tsis zoo cuam tshuam nrog kev noj turmeric thaum lub sijhawm 2-hli mus sim [17]. Qhov nce ROS tuaj yeem ua rau IL-8 ntau lawm thiab ua rau txo qis glutathione, uas tuaj yeem yog vim muaj OS ntau ntxiv los ntawm kev mob hauv ESRD cov neeg mob uas muaj thiab tsis muaj ntshav qab zib mellitus [91]. Tsis tas li ntawd, redox imbalance tseem ceeb heev rau TGF- ntau lawm [47], uas tau ntev tau suav tias yog tus neeg nruab nrab ntawm lub raum fibrosis.

Lwm txoj kev tshawb fawb qhia txog kev ua tau zoo thiab kev nyab xeeb ntawm turmeric hauv kev txo qis uric pruritus (UP) thiab hs-CRP hauv ESRD cov neeg mob. Txawm li cas los xij, cov kws sau ntawv tau piav qhia tias tus qauv loj dua thiab lub sijhawm kho mob ntev dua yuav tsum tau ntxiv kom paub meej tias qhov ua tau zoo thiab kev nyab xeeb ntawm kev ntxiv turmeric hauv cov neeg mob hemodialysis (HD) [18]. Kev tshuaj xyuas pom tau tias curcumin, ua antioxidant, txo lub raum mob thiab tuaj yeem tiv thaiv cov teeb meem ntawm ntshav qab zib mellitus [92]. Nws tau raug pom tias nws yog ib qho kev pabcuam ruaj ntseg rau kev txhim kho macroscopic proteinuria hauv cov neeg mob T2DM [93].

Lwm cov kev tshawb fawb kuj tau qhia tias curcumin yog ib qho kev kho mob zoo rau kev txo qis macroscopic proteinuria, raws li tau pom nyob rau hauv ib qho kev sim tshuaj ntsuam xyuas ob qhov muag tsis pom kev ua rau 46 tus neeg mob T2DM. Hauv txoj kev tshawb no, cov neeg mob tau txais 500 mg (ib ntsiav tshuaj) ntawm curcumin peb zaug / hnub tom qab noj mov rau 16 lub lis piam. [94]. Cov kws tshawb fawb tau hais tias qhov ntau ntawm cov proteinuria tsis tu ncua tau cuam tshuam nrog rau qib ntawm kev ua kom tsis zoo ntawm creatinine tshem tawm; curcumin txo qis creatinine tshem tawm, ua rau lub raum ua haujlwm qeeb qeeb thiab, tejzaum nws rov qab los ntawm fibrotic raug mob [94]. Ntxiv nrog rau 6 g ntawm turmeric augmented postprandial serum insulin ntau ntau tab sis tsis zoo li cuam tshuam rau cov ntshav qabzib qib lossis glycemic Performance index hauv cov neeg noj qab haus huv. Cov txiaj ntsig no qhia tau hais tias turmeric tuaj yeem ua rau cov tshuaj insulin secretion [95]. Ntawm qhov tod tes, hauv kev tshawb nrhiav kev sim, cov kws tshawb fawb tau pom tias curcumin txo qis lipid peroxidation hauv cov ntshav ntawm cov neeg uas tsis muaj ntshav qab zib lossis ntshav qab zib mellitus CKD thiab txhim kho cov tshuaj tiv thaiv antioxidant hauv cov neeg mob ntshav qab zib proteinuric CKD, ua kom pom tias kev noj zaub mov noj ntawm cov turmeric muaj cov tshuaj tiv thaiv antioxidant. muaj peev xwm antioxidant nyhuv hauv cov neeg mob uas tsis yog mob ntshav qab zib lossis ntshav qab zib mellitus CKD [15].

Tsis tas li ntawd, ib qho randomized placebo-tswj kev sim tshuaj xyuas cov teebmeem ntawm curcumin thiab quercetin ntawm kev ua haujlwm ntxov ntxov hauv 43 tus neeg tau txais kev lim ntshav-dependent cadaveric raum. Ib ntsiav tshuaj ntawm curcumin (480 mg) thiab quercetin (20 mg) tau muab rau cov neeg mob rau 1 lub hlis tom qab kev hloov pauv. Cov instigators ntawm tsab ntawv ceeb toom no tau xaus lus tias curcumin thiab quercetin tuaj yeem rov qab tau cov txiaj ntsig ntxov hauv cadaveric raum hloov, tej zaum los ntawm kev ua kom muaj heme oxygenase-1 (HO-1) [19]. Zoo li kev siv cov khoom muaj txiaj ntsig zoo ntawm cov bioflavonoids no yog kev ua haujlwm ntawm HO-1, ib qho enzyme inducible uas tsim cov pa roj carbon monoxide. Kev txhawb nqa ntawm HO-1 hauv kev hloov pauv hauv nruab nrog cev muaj peev xwm txo qis ischemia-reperfusion (IR) kev puas tsuaj thiab alloimmunity. Tsis tas li ntawd, curcumin induced HO-1 mRNA nyob rau hauv tib neeg proximal tubule raum hlwb [96], thiab qhov induction no tej zaum yuav yog nyob ntawm cov khoom nuclear erythroid 2-txog yam 2 (Nrf2) transcription factor [97].

Ib yam nkaus li, kev tswj hwm turmeric luv luv tuaj yeem txo qis hematuria, proteinuria, thiab ntshav siab systolic hauv cov neeg mob uas rov qab los yog refractory lupus nephritis, raws li tsim nyob rau hauv randomized thiab placebo-tswj sim ntawm 24 tus neeg mob nrog qhov kev kuaj mob no. Txhua tus neeg mob hauv pawg kuaj tau muab ib lub tshuaj ntsiav rau 3 lub hlis, muab 500 mg turmeric, 22.1 mg ntawm cov ntsiab lus tseem ceeb curcumin (peb ntsiav tshuaj txhua hnub). Txawm li cas los xij, kev sim mus sij hawm ntev nrog kev siv tshuaj ntau dua ntawm turmeric yuav tsum tau qhia nws cov txiaj ntsig ntawm lub raum kev ua haujlwm ntawm cov neeg mob no thiab tus nqi ntawm kev loj hlob ntawm CKD ntawm txawv keeb kwm [17]. Txawm li cas los xij, kev tshawb fawb ntxiv tau pom zoo los ntsuas qhov kev nyab xeeb luv luv thiab ntev thiab kev ua tau zoo ntawm curcumin hauv pawg kawm no [98].

3.2.9 ib. Epicatechin-3-gallate, Epicatechin, Epigallocatechin

Polyphenolic constituents (los ntawm tshuaj yej tsob nroj; Camellia sinensis) muaj siab tiv thaiv inflammatory, antioxidant, thiab antimutagenic zog nyob rau hauv ntau yam kab mob lom. Polyphenols tso saib cov khoom muaj txiaj ntsig kev noj qab haus huv rau cov kab mob ntev, suav nrog CKD [99]. Feem ntau ntawm cov khoom xyaw hauv tshuaj yej (ntawm 400 chemicals uas tau txheeb xyuas) yog polyphenolic tebchaw, tshwj xeeb tshaj yog flavonoids los ntawm cov tshuaj yej tsob nroj (Camellia sinensis), uas yog siab nyob rau hauv catechin (flavonoid subtype). Peb qhov loj catechins pom hauv cov tshuaj yej ntsuab tau piav qhia: epicatechin, epigallocatechin, thiab epicatechin-3-gallate (EGCG). Qhov ntau tshaj plaws thiab tshawb nrhiav catechin yog EGCG [99]. Nyob rau lub sijhawm tsis ntev los no, muaj peev xwm siv EGCG hauv kev kho mob thiab tiv thaiv ntau yam kab mob raum, uas feem ntau cuam tshuam nrog kev mob thiab oxidative kev nyuaj siab tau raug tshuaj xyuas [100].

Cov tshuaj tiv thaiv kab mob antioxidant, tiv thaiv kab mob, thiab kev ua haujlwm antiapoptotic ntawm EGCG tuav kev cia siab rau nws txoj kev siv los ua lwm txoj hauv kev los tswj lossis tiv thaiv ntau yam kab mob raum. Cov txiaj ntsig zoo ntawm EGCG yog kho los ntawm cov txheej txheem molecular hauv qab, feem ntau yog los ntawm kev cuam tshuam ncaj qha ntawm kev ntxhov siab lossis kev txhawb nqa-vim ROS overproduction; Tsis tas li ntawd, nws tuaj yeem cuam tshuam rau Nrf2-Keap1-Cul-3 complex, ua rau muaj kev hloov pauv nuclear ntawm Nrf2 dawb, tom qab khi rau cov tshuaj tiv thaiv antioxidant (ARE) hauv thaj tsam txhawb nqa ntawm cov cytoprotective genes thiab cov encoding antioxidant enzymes, uas zoo ib yam li modulated los ntawm NF-κB signaling pathways. Txawm li cas los xij, feem ntau ntawm tag nrho cov kev tshawb fawb siv EGCG lossis tshuaj yej ntsuab hauv cov kab mob raum tau nyob hauv cov qauv tsiaj lossis kab lis kev cai ntawm tes. Yog li, cov kev tshawb fawb soj ntsuam yuav tsum tau txais kev txhawb nqa kev tshawb fawb rau cov khoom renoprotective ntawm EGCG ntawm lub raum pathologies [101,102].

Hauv lwm cov kev tshawb fawb, cov kws sau ntawv tau ntsuas qhov ua tau ntawm kev siv cov sib xyaw ntawm EGCG thiab amla extract (AE) tau los ntawm Emblica Officinalis, Indian gooseberry, hauv kev kho mob ntawm uremic cov ntsiab lus nrog T2DM. Ib ntsiav tshuaj EGCG / AE tau muab tshuaj rau qhov ncauj (ib ntsiav tshuaj peb zaug hauv ib hnub) rau cov neeg mob ntshav qab zib uremic rau 3 lub hlis, siv tag nrho cov koob tshuaj txhua hnub ntawm 300 mg ntawm EGCG thiab 300 mg ntawm AE / hnub. Cov txiaj ntsig tau pom tias 1: 1 EGCG / AE txhim kho cov ntshav qab zib biomarkers, tiv thaiv antioxidant, thiab qhov ntsuas atherogenic hauv cov neeg mob ntshav qab zib uremic. Raws li cov txiaj ntsig no, cov kws tshawb fawb tau txiav txim siab tias EGCG thiab AE muaj peev xwm siv tau rau hauv kev kho cov neeg mob ntshav qab zib hauv lub xeev uremic [21,103].

3.2.10. Pomegranate (Punica granatum)

Cov txiv hmab txiv ntoo uas raug xaiv los ua "ib yam tshuaj hauv nws tus kheej" uas tau ntev tau suav nrog hauv cov tshuaj kho mob rau kev tiv thaiv thiab kho mob [83]. Nws muaj cov ntsiab lus siab ntawm polyphenols, alkaloids, thiab anthocyanins (flavonoid antioxidants), uas muaj txiaj ntsig zoo ntawm kev tshem tawm cov dawb radicals [104,105]. Cov teebmeem nephroprotective ntawm pomegranate extract ntawm calcium uas muaj lithiasis txoj kev loj hlob hauv cov neeg mob hnub nyoog 18 txog 70 xyoo nrog cov pob zeb rov tshwm sim tau raug tshuaj xyuas. Kev tswj hwm txhua hnub ntawm pomegranate extract tau txhawb nqa qhov tseem ceeb hauv cov ntshav paraoxonase1 (PON1), nrog rau kev txo qis hauv calcium oxalate supersaturation. PON1 yog cov tshuaj tiv thaiv atherosclerotic cuam tshuam nrog high-density lipoprotein (HDL). Lub luag haujlwm tseem ceeb ntawm PON1 yog los tiv thaiv oxidation ntawm HDL thiab LDL [106]. Tsawg theem ntawm PON1 tau cuam tshuam nrog hypercholesterolemia, ntshav qab zib, thiab kab mob vascular. Kev txhawb nqa los ntawm cov kev tshawb pom saum toj no, cov kws tshawb fawb qhia tias lub tswv yim no tuaj yeem tswj tau qhov kev pheej hmoo ntawm lub raum pob zeb loj hlob [23].

3.2.11. Resveratrol

Nws yog ib yam khoom phenolic (ib qho uas tsis yog-flavonoid stilbene polyphenol), thiab cov trans-isomer yog suav tias yog cov khoom siv roj ntsha tshaj plaws. Ntau qhov kev soj ntsuam hauv tsev kho mob thiab chaw kho mob tau lees paub cov tshuaj tiv thaiv kab mob, tshuaj tiv thaiv kab mob, hepatoprotective, neuroprotective, anticancer, thiab antioxidant zog ntawm resveratrol (RSV; 3,5,40 -trihydroxystilbene). Zoo li kev txawj ntse, kev txhawb nqa hauv vivo thiab hauv vitro kev sim ntawm RSV hauv lub raum puas tau qhia tias nws tuaj yeem txo cov fibrosis, mesangial expansion, OS, thiab inflammatory cytokine theem thaum txhim kho lub raum qauv thiab kev ua haujlwm [107]. Tsis tas li ntawd, nrog rau lub hom phiaj ntawm kev soj ntsuam cov kev ua ntawm RSV cov thawj coj ntawm Nrf2 thiab NF-κB qhia hauv cov neeg mob uas tsis tau lim ntshav nrog CKD, cov neeg tshawb xyuas tau ua qhov kev sim ua ob qhov muag tsis pom kev sib tw hauv 20 tus neeg mob uas tsis tau lim ntshav nrog CKD, thiab lawv cov txiaj ntsig tau pom tias Kev tswj hwm RSV ntawm koob tshuaj 500 mg ib hnub rau lub sijhawm 4 lub lis piam tsis muaj cov tshuaj tiv thaiv kab mob lossis tshuaj tiv thaiv kab mob hauv cov ntsiab lus no [108]. Ntawm qhov tod tes, nyob rau hauv lwm qhov kev sim ua ob qhov muag tsis pom kev, cov neeg mob ntshav qab zib peritoneal tau muab tshuaj tsawg (150 mg / hnub) lossis siab (450 mg / hnub) koob tshuaj trans-resveratrol dhau 12 lub lis piam, ua rau muaj kev sib zog ntawm qhov nruab nrab. Ultrafiltration (UF) ntim thiab qib. Ntxiv mus, angiogenesis biomarkers, VEGF, fetal siab kinase -1 (Flk-1), thiab angiopoietin (Ang) -2 tus nqi hauv peritoneal dialysate effluent (PDE) tau poob qis hauv cov neeg mob kho nrog. koob tshuaj ntau ntawm RSV, thaum theem ntawm angiopoietin receptor (Tie-2) thiab thrombospondin-1 (Tsp-1) hauv cov dej ntws tau ntxiv nrog kev kho RSV. Cov ntaub ntawv no qhia tau hais tias kev tswj hwm RSV muaj cov txiaj ntsig angiogenesis-txhim kho hauv cov neeg mob PD thiab txhawb nqa lub raum ua haujlwm ultrafiltration [26]. Ntxiv mus, kev kho RSV txo qis hauv cov ntshav creatinine ntau thiab khaws GFR, qhia txog kev ua haujlwm rau lub raum. Yog li, cov kws tshawb fawb tau qhia tias RSV txo qis insulin tsis kam thiab OS thiab nce pAkt: Akt qib hauv platelets thiab tso zis ortho-tyrosine tshem tawm [25].

Ib yam li ntawd, kev tshuaj xyuas tau ua los ntawm 24 tus neeg mob kuaj pom tias muaj ntshav siab ntawm 45 thiab 65 xyoo ntawm lub hnub nyoog thiab nrog kev puas tsuaj ntawm endothelial uas tau koom nrog hauv kev sib tw ob qhov muag tsis pom kev placebo-tswj crossover sim. Txhua tus neeg mob tau noj ib koob tshuaj trans-resveratrol (300 mg) lossis ib qho placebo. Kev ntsuas ntshav siab (BP), aortic systolic ntshav siab (SBP), thiab brachial flow-mediated dilation (FMD) tau saib xyuas ua ntej thiab 1.5 teev tom qab kev cuam tshuam. Cov txiaj ntsig tseem ceeb tau tshaj tawm yog tias FMD tau nce ntxiv hauv cov poj niam tab sis tsis yog txiv neej cov neeg mob tau txais trans-resveratrol. Cov txiaj ntsig no qhia tau hais tias cov neeg mob ntshav siab uas muaj kev ua haujlwm tsis zoo endothelial, feem ntau yog cov poj niam thiab cov neeg muaj LDL-c siab, tau pom tias muaj kev txhim kho hauv endothelial kev ua haujlwm nrog ib koob ntawm trans-resveratrol, txawm hais tias tsis muaj kev txhim kho tseem ceeb hauv peripheral thiab central BP ranges [27,109] .

Tsis tas li ntawd, hauv lwm qhov kev sim tshuaj ntsuam xyuas ob qhov muag tsis pom kev siv cov placebo tswj tau ua nyob rau hauv 60 cov neeg mob uas muaj kev kuaj mob ntawm T2DM thiab albuminuria, resveratrol tau random muab tshuaj ntawm 500 mg ib hnub twg lossis cov placebo rau lub sijhawm 90 hnub, thiab losartan yog. Ntxiv nrog rau qhov koob tshuaj 12.5 mg ib hnub rau txhua qhov kev tshawb fawb. Lawv cov txiaj ntsig tau pom tias qhov nruab nrab ntawm cov zis albumin / creatinine concentration tau txo qis hauv pawg RSV, thiab tso zis albumin tshem tawm, yoo ntshav ntshav qabzib (FPG), insulin, homeostasis qauv ntsuas ntawm insulin tsis kam (HOMA IR), thiab glycosylated hemoglobin (HbA1c). tag nrho cov kev txo qis hauv RSV pawg piv nrog cov placebo pab pawg, thaum cov tshuaj tiv thaiv antioxidant ntawm RSV tau kwv yees los ntawm kev ntsuas cov ntshav ntawm SOD1, glutathione peroxidase (GSH-Px), thiab catalase (CAT). Cov neeg mob kho nrog RSV pom qhov tseem ceeb nce qib hauv cov ntshav ntawm SOD1, GSH-Px, CAT, thiab TSIS TAU piv nrog cov placebo, lees paub nws cov tshuaj tiv thaiv antioxidant. Cov kws sau ntawv tau xaus lus tias RSV tuaj yeem ua tau zoo raws li kev sib txuas rau angiotensin receptor blockers (ARBs) kom txo qis cov zis albumin tawm hauv cov neeg mob ntshav qab zib nephropathy [24].

Raws li tau hais tseg, cov txiaj ntsig kev noj qab haus huv ntawm RSV zoo li yog qhov dav, nrog txo cov kev mob tshwm sim ntawm RSV ua rau nws yog qhov kev xaiv zoo rau kev siv tshuaj tiv thaiv rau lub raum puas. Txawm li cas los xij, kev tshawb fawb ntxiv thiab kev sim tshuaj ntsuam xyuas yog qhov tseem ceeb rau kev nkag siab tag nrho cov kev ua ntawm RSV ntawm lub raum raug mob [107,110].

3.2.12. Sulforaphane

Nws yog ib qho bioactive tivthaiv uas yog ib tug precursor ntawm glucosinolate nyob rau hauv cruciferous zaub, tshwj xeeb tshaj yog nyob rau hauv cov tub ntxhais hluas broccoli sprouts (BS) [111,112]. Qhov ua tau zoo ntawm sulforaphane (SFN; 1-isothiocyanate-4-methyl-sulphinyl butane) hauv CKD koom nrog kev tiv thaiv lossis txo qis ntawm cov qauv raug mob thiab hloov pauv hauv lub raum ua haujlwm; qhov txo qis ntawm cov proteinuria los ntawm kev ua kom tsis zoo los ntawm kev nce mRNA qhia ntawm Nrf2, NADPH quinone oxidoreductase 1 (NQO-1), HO-1, thiab SOD; thiab txo OS. Tsis tas li ntawd, cov txiaj ntsig ntawm ntau tus qauv ntawm cov kab mob hauv lub raum qhia tias SFN tuaj yeem ua rau ntau txoj hauv kev hauv lub raum puas, tshwj xeeb tshaj yog nyob rau hauv ameliorating o thiab OS, thiab yog li tuaj yeem sawv cev rau lub tswv yim ntawm kev xaiv los txhim kho qhov kev mob tshwm sim ntawm CKD cov neeg mob los ntawm kev tiv thaiv kev loj hlob. PIB [113–115].

Ib yam li ntawd, cov tshuaj BS tau ua lag luam ntev ntev rau cov txiaj ntsig kev noj qab haus huv ntawm SFN, uas ua rau NrF2 txoj hauv kev thiab cov noob caj noob ces qis, suav nrog Phase 2 enzymes. Cov khoom lag luam BS feem ntau muaj BS ntim raws li glucoraphanin (GR), uas yog hydrolyzed rau SFN los ntawm plab hnyuv microbiota, uas synchronously augments cov dej num ntawm Phase 2 enzymes xws li NQO1 thiab glutathione S-transferase (GST), thiab kuj Nrf2 signaling. , nyob rau hauv ntau cov ntaub so ntswg tib neeg. Cov kws tshawb fawb tau pom tias cov koob tshuaj tsawg (30 mg ib hnub) ntawm GF muaj cov tshuaj tiv thaiv zoo rau tib neeg [99]. Ib yam li ntawd, cov teebmeem antioxidant raug ntaus nqi rau SF, raws li qhia nyob rau hauv ib tug randomized placebo-tswj ob-dig muag mus sib hais nyob rau hauv cov txiv neej cov neeg mob kuaj pom muaj rog daim siab. Qhov kev tshawb fawb no tau qhia tias kev noj zaub mov ntxiv nrog BS extract suav nrog SF precursor GR zoo li yuav ua tiav hauv kev txhim kho lub siab ua haujlwm los ntawm kev txo qis ntawm OS txoj hauv kev [100]. Ib yam li ntawd, kev tshawb fawb soj ntsuam tau ua los soj ntsuam cov tshuaj tiv thaiv kab mob ntawm BS hmoov (BSP) nrog cov ntsiab lus sulforaphane siab, uas cov kws tshawb fawb tau soj ntsuam cov kab mob biomarkers hauv cov neeg mob kuaj mob T2DM, uas tau muab faib ua peb txoj kev kho mob. pab pawg rau 4 lub lis piam. Cov pab pawg tau txais 10 g / d BSP (n=27), 5 g / d BSP (n=29), lossis placebo (n=25). Cov txiaj ntsig tau pom tias cov ntshav siab C reactive protein (hs-CRP) thiab interleukin-6 (IL{22}}) qis dua hauv pawg A (10 g / d koob) piv nrog pawg tswj hwm tom qab- kev cuam tshuam. Qhov no tau qhia tias sulforaphane-nplua nuj BSP muaj cov txiaj ntsig zoo ntawm cov kab mob inflammatory hauv cov neeg mob T2DM [28]. Ntawm qhov tod tes, kev tshawb fawb soj ntsuam tau soj ntsuam cov kev ua ntawm kev ncua ntev nrog BS ntawm cov kab mob inflammatory (TNF- , IL-6, IL-1 , thiab CRP) hauv 40 yam kev noj qab haus huv. Cov theem kho mob koom nrog BS kev tswj hwm ntawm koob tshuaj 30 g ib hnub rau 10 lub lis piam thiab cov theem tom qab yog 10 lub lis piam ntawm kev noj zaub mov tsis zoo thiab noj BS dawb. Cov txiaj ntsig tau pom tias IL-6 thiab CRP qhov tseem ceeb tau txo qis heev nyob rau hauv lub sijhawm tswj hwm thiab tias cov cim kev mob tshwm sim tau khaws cia qis [116]. Tsis tas li ntawd, cov kws tshawb fawb tau tshawb fawb txog cov tshuaj tiv thaiv kab mob ntawm SF hauv kev tshawb fawb randomized nyob rau hauv cov tub ntxhais hluas noj qab haus huv thiab ua kom pom qhov cuam tshuam ntawm cov zaub cruciferous nrog cov ntsiab lus SF siab ntawm cov kab mob ntshav qab zib tshwj xeeb, tshwj xeeb yog qhov txo qis hauv IL-6, CRP, thiab soluble TNF receptor (sTNFRI), ua tib zoo hais tias cov concentrations siab dua ntawm cov neeg uas muaj GSTM1-null genotypes [117].

4. Kev sib tham

Lub raum kab mob feem ntau tshwm sim nyob rau lub sijhawm, yog li nws tsis yog feem ntau kuaj pom kom txog thaum lub raum ua haujlwm tsis zoo. Pathophysiologically, CKD yog qhov tshwm sim ntawm ntau yam kab mob pathological uas tshem tawm qee qhov nephrons; Tom qab ntawd, nephrons overcompensate nrog hyperfiltration. Nyob rau tib lub sijhawm, glomerular hypertension, albuminuria, thiab poob ntawm lub raum ua haujlwm tau tsim. Qhov nce glomerular capillary siab ua rau muaj kev puas tsuaj rau glomerular capillary endothelium, kev puas tsuaj ntawm podocytes hauv ob sab phlu capillaries, thiab nce permeability ntawm macromolecules. [118, 119]. Tsis tas li ntawd, nce pro-inflammatory moderators uas induce fibrotic cell proliferation tau koom nrog. Tsis tas li ntawd, qhov nce hauv ECM molecules ua rau muaj kev loj hlob ntawm caws pliav thiab lub raum puas [120]. Tam sim no, muaj cov txheej txheem kho mob rau CKD, nrog rau txhua txoj hauv kev uas tsom mus rau kev tshem tawm lossis tiv thaiv kev puas tsuaj, suav nrog kev siv tshuaj, kev saib xyuas kev noj qab haus huv, kev lim ntshav, thiab kev hloov pauv [121].

Kev tshawb fawb tau pom zoo tias cov zaub mov nplua nuj nyob hauv zaub thiab txiv hmab txiv ntoo pab tswj lub cev qhov hnyav thiab tiv thaiv cov kab mob ntev, nrog rau cov kab mob metabolic thiab cov hlab plawv, mob qog noj ntshav, thiab CKD [20,122,123]. Tsuas yog qee qhov kev sim siab tau txheeb xyuas bioactive compound supplementation hauv tib neeg. Kev tshawb fawb ntxiv yuav tsum tau ua los tsim kom muaj qhov zoo tshaj plaws thiab txoj kev tswj hwm ntawm bioactive compounds [114,115]. Tsis tas li ntawd, kev tshawb nrhiav yav tom ntej yuav tsum tau coj mus rau kev txheeb xyuas qhov tshwj xeeb teeb liab / cellular mechanisms modulated los ntawm bioactive compounds uas pab txhawb kev tiv thaiv lossis txo qis ntawm lub raum puas. Kev tshawb nrhiav ntxiv kuj tseem xav tau los ntsuas cov tshuaj pharmacokinetic ntawm cov tshuaj bioactive, xws li txoj hauv kev zoo tshaj plaws ntawm kev tswj hwm, ntau npaum li cas thiab bioavailability, cov metabolism, cov ntaub so ntswg faib, thiab tshem tawm, thiab cov tshuaj pharmacodynamic, xws li molecular mechanisms ntawm kev ua ntawm bioactive compounds, Qhia lawv cov kev ua tau zoo thiab kev nyab xeeb nyob rau lub sijhawm luv thiab ntev hauv kev tshawb fawb soj ntsuam.

5. Cov lus xaus

Qhov kev tshuaj xyuas no qhia txog qhov muaj txiaj ntsig zoo ntawm bioactive tshuaj nroj tsuag cov tebchaw hauv kev txhim kho lub raum ua haujlwm. Txhua yam-natural compounds piav qhia hauv daim ntawv tshaj tawm no zoo li muaj qee qhov txiaj ntsig hauv kev txhim kho OS, mob, thiab muaj peev xwm antioxidant. Ntau NPCs txo cov fibrosis vim hyperglycemia-induced OS, attenuate proteinuria, txo hematuria thiab systolic ntshav siab, thiab siv cov tshuaj tiv thaiv nephrotoxic, thiab yog li lawv tau cog lus cov cuab yeej kho mob los txo lossis tiv thaiv qhov pib thiab kev nce qib ntawm KD pathogenesis. Ntuj bioactive compounds raug txiav txim siab los ua haujlwm tseem ceeb hauv txoj hauv kev ntawm kev siv tshuab thiab kom muaj cov txiaj ntsig kho mob tau zoo; Txawm li cas los xij, kev tshawb nrhiav ntxiv yog tsim nyog kom tau txais kev nkag siab tob dua ntawm lawv cov haujlwm tshwj xeeb pathophysiological, thiab kev ntsuam xyuas ntawm cov teebmeem no hauv kev sim loj dua yog xav pom zoo.

Sau Kev Koom Tes: Kev Tsim Nyog, LA-C., thiab MLM-F.; methodology, GTG-M.; EAG-M.; IG-V.; validation, LA-C.; GTG-M. thiab MLM-F.; kev soj ntsuam, GTG-M.; LA-C.; IG-V.; kev tshawb nrhiav, GTG-M.; DLD-A.; LA-C.; MLM-F.; EAG-M.; IG-V.; cov ntaub ntawv, MLM-F.; sau ntawv—kev npaj ua ntej, LA-C.; sau ntawv—kev tshuaj xyuas thiab kho, LA-C.; DLD-A.; MLM-F.; IG-V.; GTG-M.; Visualization, LA-C.; MLM-F.; IG-V.; saib xyuas, EAG-M.; project tswj, MLM-F. Txhua tus kws sau ntawv tau nyeem thiab pom zoo rau cov ntawv luam tawm ntawm cov ntawv sau. Cov Nyiaj Txiag: Qhov kev tshawb fawb no tau txais tsis muaj nyiaj txiag sab nraud.Institutional Review Board Statement: Tsis siv tau.Informed Consent Statement: Tsis siv tau.Data Availability Statement: Tsis muaj.Conflicts of paj: Cov sau ntawv tshaj tawm tsis muaj teeb meem ntawm paj.

Lorena Avila-Carrasco 1,2,*, Elda Araceli García-Mayorga 2, Daisy L. Díaz-Avila 2, Idalia Garza-Veloz 1, Margarita L Martinez-Fierro 1 thiab Guadalupe T González-Mateo 3,4

1 Molecular Medicine Laboratory, Academic Unit of Human Medicine and Health Sciences, AutonomousUniversity of Zacatecas, Carretera Zacatecas-Guadalajara Km.6, Ejido la Escondida, Zacatecas 98160, Mexico;

2 Academic Unit of Human Medicine and Health Sciences, Therapeutic and Pharmacology Department, Autonomous University of Zacatecas, Zacatecas 98160, Mexico; emayorga3@gmail.com (EAG-M.);

3 Kev Tshawb Fawb Lub Tsev Kawm Ntawv ntawm La Paz (IdiPAZ), University Tsev Kho Mob La Paz, 28046 Madrid, Spain;

4 Molecular Biology Research, Center Severo Ochoa, Spanish Council rau Kev Tshawb Fawb Txog Kev Tshawb Fawb (CSIC), 28049 Madrid, Spain *

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