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Kev paub

Tiv thaiv cov nyhuv ntawm Dub cumin thiab nws cov khoom xyaw nquag ntawm lub raum raug mob

Mar 20, 2022

Md. Abdul Hannan1,2, Md. Sarwar Zahan1, Partha Protim Sarker 1, Akhi Moni 1, Hunjoo Ha 3 and Md Jamal Uddin1,3,*



Abstract:Qhov nthuav dav ntawmmob ntevraumkab mob(CKD) tau nce thoob ntiaj teb, thiab kev sib raug zoo ntawmmob hnyavraumraug mob(AKI) thiab CKD tsis ntev los no tau txheeb xyuas.Dub cumin(Nigella sativa) tau pom tias muaj txiaj ntsig zoo hauv kev kho ntau yam kab mob raum. Cov ntaub ntawv pov thawj qhia tau tias cov cumin dub thiab nws cov khoom tseem ceeb, thymoquinone (TQ), tuaj yeem tiv thaiv lub raum raug mob los ntawm ntau yam xenobiotics, uas yog cov tshuaj tua kab mob, cov hlau hnyav, tshuaj tua kab, thiab lwm yam tshuaj ib puag ncig. Dub cumin kuj tuaj yeem tiv thaiv lub raum los ntawm ischemic shock. Cov txheej txheem hauv qab ntawm lub raum tiv thaiv muaj peev xwm ntawm cov cumin dub thiab TQ suav nrog kev tiv thaiv oxidation, tiv thaiv kab mob, tiv thaiv apoptosis, thiab tshuaj tiv thaiv kab mob uas tau tshwm sim hauv lawv txoj haujlwm tswj hwm kev tiv thaiv antioxidant, NF-kB signaling, caspase pathways, thiab TGF- signaling. . Hauv kev sim tshuaj, cov roj noob dub tau pom tias ua rau cov ntshav thiab zis tsis zoo thiab txhim kho cov txiaj ntsig ntawm cov neeg mob CKD. Thaum cov cumin dub thiab nws cov khoom tau pom tias muaj txiaj ntsig zoo rau lub raum kev tiv thaiv, cov ntaub ntawv ntawm nanoparticle-coj coj mus rau hauv lub raum tseem tsis muaj. Ntxiv mus, cov pov thawj kho mob ntawm cov khoom ntuj no tsis txaus los pom zoo rau cov neeg mob CKD. Qhov kev tshuaj xyuas no muab cov ntaub ntawv nkag siab txog cov txiaj ntsig ntawm pharmacological ntawm dub cumin thiab TQ tiv thaiv lub raum puas.


Ntsiab lus:dub cumin;raumraug mob; nephrotoxicity; thymoquinone; xenobiotic kev nyuaj siab

Hu rau: ali.ma@wecistanche.com

to prevent chronic kidney disease by black cumin

1. Taw qhia

Lub raumCov kab mob raug suav hais tias yog teeb meem kev noj qab haus huv thoob ntiaj teb.Mob raum mob(CKD) yog tus tswj xyuas qhov tseem ceeb ntawm kev mob thiab kev tuag los ntawm cov kab mob tsis sib kis, thaum qhov tshwm sim ntawm mob raum raug mob (AKI) tau nce thoob ntiaj teb [1]. Cov neeg mob uas muaj keeb kwm ntawm AKI tuaj yeem tsim CKD [2,3]. Lub pathophysiology ntawm lub raum kab mob yog complex thiab muaj xws li mob, tubular raug mob, thiab vascular puas [4,5]. Raws li cov kab mob excretory, ob lub raum yog qhov tshwj xeeb tshaj yog cuam tshuam rau cov tshuaj lom xenobiotics thiab lawv cov metabolites. Nrog rau kev nthuav dav ntxiv rau xenobiotics xws li tshuaj, co toxins, thiab cov tshuaj ib puag ncig, lub ntiaj teb tshwm sim ntawm cov kab mob tib neeg mob xws li kab mob raum tau loj hlob ntawm qhov txaus ntshai [6]. Xenobiotics cuam tshuam cov qauv thiab kev ua haujlwm ntawm lub raum los ntawm kev ua rau oxidative kev nyuaj siab, o, apoptosis, thiab fibrosis, ua rau kev loj hlob ntawm AKI thiab CKD [6,7]. Txawm hais tias pathophysiology ntawm ntau yam kab mob raum tau kawm, ntau lub hom phiaj kho mob tau ua tsis tiav [8]. Yog li, yuav tsum muaj kev cuam tshuam sai los kho cov neeg mob raum.

the best herb for kidney disease

Dub cumin(Nigella sativa L.) yog ib hom tshuaj ntsim ntsim thiab nws cov noob, tshwj xeeb tshaj yog, ib txwm tau qhia txog kev tswj hwm ntawm ntau tus neeg mob, suav nrog cov cuam tshuam rau lub raum [9]. Thymoquinone (TQ), lub luag haujlwm tseem ceeb ntawm cov noob cumin dub thiab nws cov roj, tau pom los txhawb kev ua haujlwm ntawm cov kabmob sib txawv, suav nrograumua haujlwm [10]. Cov pov thawj Mounting qhia tau hais tias cov cumin dub thiab TQ tuaj yeem txo cov teeb meem rau lub raum los ntawm ntau yam kev ntxhov siab, xws li cov kws khomob, cov tshuaj metabolic tsis txaus, thiab cov tshuaj lom ib puag ncig [11]. Cov ntaub ntawv pov thawj los ntawm cov kev tshawb fawb preclinical tau pom tias cov noob cumin dub (hauv daim ntawv ntawm hmoov, rho tawm, lossis roj) thiab TQ tiv thaiv kev raug mob raum los ntawm ischemia [12,13], tshuaj kho mob qog noj ntshav (methotrexate thiab cisplatin) [14,15] ], tshuaj tua kab mob (paracetamol, acetylsalicylic acid, thiab aspirin) [16–18], hnyav hlau (arsenic thiab cadmium) [19,20], tshuaj tua kab (miconazole thiab diazinon) [21,22], thiab lwm yam tshuaj (carbon tetrachloride thiab sodium nitrite) [23,24]. Cov ntaub ntawv pov thawj, txawm tias txwv, kuj qhia txog kev txhim kho kev kho mob hauv cov neeg mob CKD kho nrogdub cumin[25–27]. Tsis tas li ntawd,dub cumintau pom tias muaj txiaj ntsig zoo hauv kev hloov kho ntau yam kev pheej hmoo rau mob raum xws li kub siab, atherosclerosis, dyslipidemia, hyperglycemia, thiab ntshav qab zib [11]. Lub raum-tiv thaiv cov teebmeem ntawm cov cumin dub yog vim nws cov tshuaj tiv thaiv kab mob antioxidant, tiv thaiv inflammatory, immunomodulatory, antiapoptotic, thiab antifibrotic zog [11,28,29]. Nyob rau hauv qhov kev tshuaj xyuas no, peb muab ib tug luv luv account ntawm kev tiv thaiv los ntawm dub cumin tiv thaiv ntau yam kev raug mob raum thiab sib tham txog molecular mechanisms yog hais tias ua tau.



2. Txoj kev

Cov ntaub ntawv tshawb fawb hauv online, xws li PubMed, Google Scholar, Scopus, thiab Lub Vev Xaib ntawm Kev Tshawb Fawb tau tshawb nrhiav los khaws cov ntaub ntawv siv cov ntsiab lus, suav nrog cov cumin dub, N. Sativa, cov roj tseem ceeb, thymoquinone,raumKev raug mob, oxidative stress, o, fibrosis, nephrotoxicity, thiab xenobiotic stress. Ob qho kev tshawb fawb preclinical thiab kho mob tau raug sau tseg. Cov ntaub ntawv luam tawm ua lwm yam tsis yog lus Askiv raug cais tawm ntawm qhov kev tshuaj xyuas no. Tag nrho cov duab tau tsim los ntawm Microsoft Powerpoint.


acteoside in cistanche have good effcts to antioxidant

3. Antioxidant thiab Anti-Inflammatory Effects ntawm Dub Cumin thiab TQ

Oxidative stress thiab o yog ob yam kab mob tshwm sim uas paub tias muaj feem cuam tshuam rau hauv pathobiology ntawm ntau yam teeb meem rau lub raum, suav nrog raum toxicity, AKI, thiab CKD [30,31]. Ntau yam khoom ntuj tsim tau pov thawj muaj peev xwm los txo cov kev ntxhov siab oxidative thiab o [32,33] thiab tau pom tias muaj txiaj ntsig tiv thaiv kab mob raum (Daim duab 1 thiab 2).

Cov ntaub ntawv pov thawj zoo los ntawm kev tshawb fawb tsiaj thiab tib neeg tau lees paub qhov kev tiv thaiv ntawmdub cuminthiab TQ tiv thaiv oxidative kev nyuaj siab [28,34–38]. Dub cumin upregulated erythrocyte glutathione peroxidase (GPx), glutathione-S-transferase (GST), thiab superoxide dismutase (SOD) qib thiab ib txhij txo qis ntshav malondialdehyde (MDA) lev-els [38,39]. Hauv ob qhov kev tshawb fawb zoo sib xws, cov cumin dub tau nce qib ntawm cov enzymes antioxidant, xws li SOD thiab catalase (CAT), thiab antioxidant molecules, xws li glutathione (GSH) thiab txo qis reactive oxygen hom (ROS) [40,41]. Ntxiv mus, N. Sativa roj (NSO) txo chlorpyrifos-induced oxidative kev nyuaj siab los ntawm kev txo qis ROS thiab nitrous oxide ntau lawm hauv Wister nas qauv [42]. Kev noj txhua hnub ntawm TQ (5 mg / kg) rau tsib lub lis piam nce siab CAT, glutathione reductase (GR), GPx, SOD, thiab GSH qib hauv daim siab [43]. Ib yam li ntawd, TQ elevates SOD, CAT, thiab GSH qib upregulate antioxidant noob thiab downregulate pro-oxidant noob [44]. Lwm txoj kev tshawb fawb hauv luav tau qhia tias noj cov noob cumin dub (600 mg / kg) txo MDA thiab nce tag nrho cov tshuaj tiv thaiv antioxidant hauv cov ntshav [45]. Ib zaug ntxiv, kev sib xyaw ua ke ntawm TQ thiab NSO tau nthuav tawm cov peev xwm antioxidant tiv thaiv cisplatin (CP) vim qhov txawv txav [46]. Ib daim ntawv qhia txog kev txheeb xyuas ntawm cov noob cumin dub tau pom cov qib SOD txhim kho yam tsis muaj qhov pom ntawm MDA qib thiab tag nrho cov peev xwm antioxidant [47]. Txawm li cas los xij, cov pov thawj preclinical ntawm cov teebmeem antioxidant ntawm dub cumin tau piav qhia hauv cov kev tshawb fawb soj ntsuam. Kev sib xyaw ua ke ntawm cov noob cumin dub thiab Allium sativum tshaj li yim lub lis piam txhim kho antioxidant hauv 30 postmenopausal, cov poj niam noj qab haus huv [39]. Ntxiv dua thiab, ntxiv NSO thiab cov khoom noj muaj calorie tsawg pom tau tias muaj kev txhim kho hauv cov tshuaj tiv thaiv antioxidant hauv kev sim tshuaj ntawm 50 tus neeg rog rog rog [48].

Nrog rau kev tiv thaiv oxidative kev nyuaj siab,dub cuminthiab TQ tau pom tias tiv thaiv kab mob raws li tau thov los ntawm cov ntaub ntawv yav dhau los [9,28,35,49]. Cov extracts thiab bioactive compounds ntawm dub cumin, xws li TQ, nigellone, thiab -hederin qhia anti-histaminic, anti-immunoglobulin, anti-leukotrienes, anti-eosinophilic, thiab anti-inflammatory teebmeem nyob rau hauv ntau yam qauv [50]. Tsis tas li ntawd, TQ suppressed pro-inflammatory yam xws li nitric oxide (NO), nitric oxide synthase (iNOS), qog necrosis factor-alpha (TNF- ), interleukin -1 beta (IL-1 ), interleukin{16}} (IL-6), thiab cyclooxygenase 2 (COX{19}}) los ntawm inhibiting IRAK-txuas AP-1/NF-kB txoj kev [51]. Hauv tib neeg cov ntshav, NSO thiab TQ inhibited 5-lipoxygenase (5-LOX) thiab leukotriene C4 synthase (LTC4S) [52], uas tuaj yeem tsim cov kab mob sib kis xws li leukotrienes thiab prostaglandins [52,53]. Hauv lwm txoj kev tshawb fawb, TQ inhibited TANK-binding kinase 1 (TBK1), txo qis hom I interferons (IFN) mRNA qhia, thiab txo qis cov kev tswj hwm interferon 3 (IRF-3) qhia txoj hauv kev hauv lipopolysaccharides (LPS)-stimulated. murine macrophage zoo li RAW264.7 hlwb [54]. Hauv lub ntsws cov ntaub so ntswg, kev kho NSO ua rau txo qis hauv IgG1, IgG2a, interleukin-2 (IL-2), interleukin-12 (IL-12), interleukin-10 (IL-10), IFN-y qib, thiab inflammatory cells [55]. Tsis tas li ntawd, kev tswj hwm ntawm NSO tau txo qis IL-6, txo qis IL-12, thiab TNF- qib hauv cov nas cuam tshuam nrog carrageenan-induced paw edema [56]. Ib yam li ntawd, ntxiv ntawm 10 feem pua ​​​​NSO txo qhov mob hauv paw edema nas nrog cov leucocytes tsawg dua thiab TNF- theem [49]. Ib zaug ntxiv, ib qho kev sim hauv tib neeg pre-adipocytes tau pom tias cov tshiab rho tawm thiab khaws cia NSO ua rau txo qis IL-6 thiab IL-1 qib, feem [57].

Figure 1. Protection against oxidative stress by black cumin and its constituents. Stress stimuli like CP and chlorpyrifos reduce antioxidant enzymes and elevate ROS and MDA levels, leading to oxidative stress, which was attenuated by N. sativa and TQ through a mechanism involving the upregulation of antioxidants enzymes and molecules, such as GPx, GR, SOD, CAT, and GSH and the subsequent reduction of ROS and MDA levels. CAT, Catalase; GPx, Glutathione peroxidase; GSH, Glutathione; GR, Glutathione reductase; MDA, Malondialdehyde; NSO, N. sativa oil; ROS, Reactive oxygen species; SOD, Superoxide dismutase; TQ, Thymoquinone.

4. Kev tiv thaiv ntawm Dub Cumin thiab TQ tiv thaiv kab mob raum

Dub cumin thiab TQ tau tshaj tawm kom txo tau ntau yam txawv txav uas feem ntau cuam tshuam nrog kev ua haujlwm ntawm lub cev.lub raum. Hauv ntu nram qab no, lub raum-tiv thaiv cov teebmeem ntawmdub cuminthiab TQ tau tham, qhia txog cov teebmeem hauv qab no (Tables 1 thiab 2).




4.1. Preclinical pov thawj ntawm raum tiv thaiv los ntawm Dub cumin

4.1.1. Kev tiv thaiv tshuaj tiv thaiv raum raug mob

Drug-induced nephrotoxicity yog ib qho ntawm feem ntau ua rauraumraug mob. Methotrexate (MTX, tus neeg saib xyuas kws khomob) nce MDA, thiab txo qis GSH qib hauv lub raum homogenate, thiab N. Sativa thim rov qab nws cov yeeb yam hauv cov nas nephrotoxic [14]. Nyob rau tib lub sijhawm, nws tau pom tias N. sativa nyob rau hauv qis qis tuaj yeem txhim kho kev ua tau zoo thiab kev nyab xeeb ntawm kev kho MTX hauv Wistar nas [58]. Nyob rau hauv cov txheej txheem antioxidant zoo sib xws, TQ ameliorated oxidative puas tsuaj los ntawm lwm yam tshuaj tiv thaiv kab mob CP hauv nas raum [59]. Hauv kev tshawb fawb tom qab los ntawm pab pawg tshawb fawb no, kev tswj hwm ntawm NSO (2 mL / kg bwt ntawm qhov ncauj), ua ntej thiab tom qab ib koob tshuaj CP kho (6 mg / kg bwt. ip), ua rau txo qis CP-induced nce hauv cov ntshav creatinine. thiab ntshav urea nitrogen (BUN) thiab txo qis hauv kev ua haujlwm ntawm txhuam ciam teb daim nyias nyias (BBM) enzymes hauv lub raum cortical thiab medullary homogenates, nrog rau hauv BBM vesicles cais (BBMV). Cov ntaub ntawv biochemical thiab histological no qhia txog qhov muaj peev xwm tiv thaiv NSO tiv thaiv CP-induced AKI [15]. Hauv ib qho kev tshawb fawb zoo sib xws ua los ntawm lwm pab pawg, N. Sativa noob hmoov (NSP), extract (NSE), thiab NSO ameliorated cov teebmeem ntawm CP-induced raum toxicity hauv Sprague-Dawley nas los ntawm alleviating serum qib ntawm urea, creatinine, thiab poov tshuaj. , thiab qhov nce siab ntawm Na, Na / K, vitamin D, cov khoom noj khoom haus, thiab cov enzymes antioxidant [60]. Zuag qhia tag nrho, cov kev tshawb fawb no pom tau tiasdub cumintuaj yeem ua tau zoo hauv kev txo cov kev mob tshwm sim lom, nquag ntsib hauv kev kho mob qog noj ntshav. Cov kev tshawb pom no tuaj yeem siv los tsim kev sib koom ua ke uas tuaj yeem tswj cov teeb meem hauv kev kho mob qog noj ntshav.

Penconazole yog siv dav siv tshuaj tua kab mob triazole hauv kev ua liaj ua teb, tib neeg, thiab cov kws kho tsiaj. Kev siv ntau ntawm penconazole ua rau nephrotoxicity thiabraumkev puas tsuaj. Cov khoom antioxidant ntawm N. Sativa tuaj yeem raug ntaus nqi rau ameliorating penconazole-induced nephrotoxicity hauv nas [21]. Cov kev kho mob sib txawv ntawm cov noob roj dub tiv thaiv thiab thim rov qab haloperidol-induced nephrotoxicity los ntawm depleting K ntxiv, Na ntxiv, MDA cov ntsiab lus, thiab aldose-reductase (AR) kev ua, thiab AMP hydrolysis nrog nce adenosine triphosphate (ATP) hauv nas raum [61]. Kev tiv thaiv ntawm N. Sativa tau raug tshuaj xyuas ntawm 4-Nonylphenol (4-NP)-induced nephrotoxicity hauv Clarias gariepinus ntses. Kev tswj hwm ntawm N. Sativa tau txo qis qhov cuam tshuam nephrotoxic ntawm {{8}NP thiab tswj lub raum qauv thiab kev ua haujlwm [62]. N. Sativa kuj tau pom tias muaj kev tiv thaiv nephrotoxicity tshwm sim los ntawm feem ntau siv cov tshuaj uas tsis yog-steroidal los tiv thaiv kab mob xws li acetylsalicylic acid [18], aspirin [17], thiab paracetamol [16]

Ib qho kev tshawb fawb tau tsim los ntsuas qhovraumKev tiv thaiv muaj peev xwm ntawm NSO tiv thaiv thioacetamide (TAA)-induced nephrotoxicity hauv nas. Cov txiaj ntsig tau lees paub tias kev kho mob ntawm NSO tseem ceeb thim rov qab TAA-siab lipid profile, urea, creatinine, uric acid, sodium, thiab potassium ntau hauv cov ntshav [63]. Yog li, kev sib xyaw ua ke ntawm metformin thiab NSO tau pom tias muaj txiaj ntsig zoo tiv thaiv TAA-induced hepatorenal toxicity hauv nas [64].

Figure 2. Protection against inflammation by black cumin and its constituents. Stimulation of various extrinsic and intrinsic stressors triggers inflammatory signals. Activity of inflammatory enzymes such as 5-LOX and LTC4S resulted in the generation of leukotrienes and prostaglandins, respectively, leading to inflammation.

4.1.2. Kev tiv thaiv Hnyav Hlau-Induced raum raug mob

Covraumyog thawj lub hom phiaj ntawm cov hlau hnyav toxicity. Kev kho mob ntawm TQ thiab ebselen (Eb) inhibited arsenic-induced oxidative puas, apoptosis, thiab o; thiab txiav txim siab txo qis arsenic txuam nrog rau hauv cov ntaub so ntswg [19]. Cov tshuaj tiv thaiv tiv thaiv kab mob hauv cov nas pretreated nrog cov cadmium (Cd)-lead (Pb) sib tov tau thim rov qab los ntawm N. Sativa hauv lub raum ntawm nas [65]. Lub peev xwm nephroprotective ntawm TQ hauv Cd toxicity tej zaum yuav yog vim nws cov khoom tiv thaiv oxidative thiab anti-apoptotic, uas yuav pab tau kom ua tiav cov txiaj ntsig zoo [20]. Cov teebmeem tiv thaiv ntawmdub cumintawm tsam Pd-induced raum raug mob tau ntxiv kev txhawb nqa los ntawm kev tshawb fawb ntawm Farrag thiab pab neeg uas tau tshaj tawm tias kev kho cov noob dub tau txo qis Pb-induced hepatorenal puas tsuaj rau txiv neej nas [66]. Zoo sib xws cov tshuaj tiv thaiv antioxidant, suav nrog induction ntawm CAT, GPx, thiab glutathione reductase kev ua ub no thiab nce hauv SOD thiab GSH qib, tau koom nrog rau kev tiv thaiv raum ntawm TQ tiv thaiv Pb-induced raum raug mob hauv nas [67].


4.1.3. Kev tiv thaiv Insecticide-Induced Kidney Injury

Diazinon yog ib hom tshuaj tua kab uas siv los tswj cov kab tsuag. Diazinon-induced oxidative kev nyuaj siab thiabraumkev ua haujlwm tsis zoo hauv cov nas. Pretreatment ntawm NSO tau hloov pauv qhov diazinon-induced hepatotoxicity thiab nephrotoxicity [22]. Fipronil yog ib qho tshuaj tua kab phenylpyrazole, dav siv rau kev ua liaj ua teb thiab tsiaj txhu. TQ thiab diallyl sulfide tiv thaiv fipronil-induced oxidativeraumkab mob hauv cov nas [68]


4.1.4. Kev tiv thaiv tshuaj lom neeg mob raum mob

Ntau yam tshuaj tuaj yeem ua rauraumraug mob. Kev tswj hwm qhov ncauj ntawm cov roj ntses ua ke thiab NSO txo cov pa roj carbon tetrachloride (CCl4) ua rau lub siab thiabraumKev raug mob hauv nas los ntawm kev tawm dag zog tiv thaiv kab mob thiab kev ua haujlwm antioxidant [69]. Cov kev tshawb pom no tau txais kev txhawb nqa los ntawm kev tshawb fawb tsis ntev los no uas pom tau tias kev tswj hwm ntawm NSO tau siv los tiv thaiv lub hlwb, lub siab, thiabraumthaum CCl4-induced oxidative stress [23].

NSO ameliorated sodium nitrite-induced nephrotoxicity los ntawm thaiv oxidative kev nyuaj siab, attenuating fibrosis thiab inflammation, restoring glycogen, ameliorating cytochrome C oxidase, thiab inhibiting apoptosis [70]. Ib yam li ntawd, kev noj TQ (25 thiab 50 mg / kg, po, txhua hnub) pom muaj kev tiv thaiv los ntawm sodium nitrite-induced.raumtoxicity nyob rau hauv cov txiv neej nas los ntawm kev txo oxidative kev nyuaj siab, restores ib txwm tshuav ntawm pro- thiab anti-inflammatory cytokines, thiab tiv thaiv raum cov ntaub so ntswg los ntawm extrinsic thiab intrinsic apoptosis [24], qhia hais tias kev tiv thaiv los ntawm NSO nyob rau hauv lub yav dhau los txoj kev tshawb no yog vim TQ- mediated antioxidant thiab anti-inflammatory teebmeem. Tsis tas li ntawd, ntxiv NSO ntawm 5 mL / kg lub cev qhov hnyav / koob tshuaj / hnub rau 28 hnub ua haujlwm nephroprotective thiab diuretic kev ua los ntawm kev txo qis cov zis thiab cov ntshav ntawm calcium, phosphate, thiab oxalate hauv Wistar nas [71], qhia txog nws cov teebmeem tiv thaiv. tiv thaiv urolithiasis.


4.1.5 ib. Kev tiv thaiv rau lub raum Ischemia/Reperfusion Injury

Lub raumischemia-reperfusion raug mob (IRI) yog tus qauv paub txog kev raug mob raum mob. Pretreatment nrog N. sativa muaj kev tiv thaiv tiv thaiv IRI-vim lub raum puas los ntawm inhibiting apoptosis thiab cell proliferation [12]. Cov nyhuv no tau txuas ntxiv los ntawm TQ supplementation (10 mg / kg / hnub) uas ua kom cov nyhuv IRI ntawm cov hemodynamic thiab tubular lub raum ua haujlwm tsis zoo, nrog rau kev qhia txog qee qhov kev raug mob raum thiab cov pro-inflammatory thiab pro-fibrotic cytokines [13] ].


4.1.6. Kev tiv thaiv tiv thaiv Urolithiasis / ureteral Obstruction

Unilateral ureteral obstruction (UUO) yog ib tug zoo-tsim qauv sim ntawmraumfibrosis. UUO muaj feem cuam tshuam rau qhov tseem ceeb hauv oxidative stress, o, thiab apoptosis [72]. N. Sativa extract yog tus neeg sawv cev kho mob los kho UUO-induced raum puas tsuaj piv nrog captopril thiab losartan [72]. Ib yam li ntawd, TQ tau txhim kho oxidative puas tsuaj, apoptosis, thiab TNF- kev qhia thiab ua rau txo qis ntawm cov tshuaj angiotensin II thiab MCP-1 piv nrog UUO nas [73].


4.1.7 ib. Tiv thaiv lwm yam kev nyuaj siab

Feem ntau cov tshuaj chemotherapeutic ua rau nephrotoxicity. Cov kev tshawb fawb tsiaj tau piav qhia txog kev tiv thaiv ntawm TQ ntawm cov tshuaj tua kab mob-induced nephrotoxicity los ntawm kev txo qis lipid peroxidation thiab ua kom muaj kev ua haujlwm ntawm cov enzymes antioxidant hauv lub cev.raumcov ntaub so ntswg ntawm kws khomob-kho tsiaj [74] Kev tshawb fawb preclinical hauv vitro tau txhais ua cov tshuaj khomob zoo dua ntawm TQ thiab nws cov analogs los khoraummob qog noj ntshav [75].

Nyob rau hauv mobraumkev raug mob tshwm sim los ntawm sepsis hauv BALB/c nas, TQ kev tswj hwm los ntawm gavage reversed CLP-induced nce nyob rau hauv cov ntshav qib ntawm CRE thiab BUN thiab cov ntaub so ntswg nthuav tawm ntawm NLRP3, caspase-1, caspase-3, caspase{{4 } }, TNF- , IL-1 , IL-6, thiab NF-kB, qhia tias TQ yuav muaj peev xwm kho tau zoo tiv thaiv sepsis-induced AKI [76]. LPS tseem yog lub luag haujlwm rau inducing sepsis-associated AKI [77,78]. TQ kho txo ​​LPS-vim lub raum fibrosis thiab permeability thiab txhim kho oxidative kev nyuaj siab [79]. TQ nthuav tawm cov teebmeem tiv thaiv ntawm hyperuricemia-mediatedraumoxidative stress thiab mitochondrial abnormalities, uas Nrf2/HO-1 tuaj yeem kho, Akt signaling pathways [80]. Hypercholesterolemia yog ib qho kev pheej hmoo zoo rau lub raum raug mob uas tuaj yeem ua rau CKD. NSO thiab TQ kev kho mob txo qis albuminuria hauv kev sim nas ntawm streptozotocin (STZ)-induced mob ntshav qab zib nephropathy los ntawm kev khaws cov podocyte muaj nuj nqi [81]. Lwm txoj kev tshawb fawb qhia tias TQ tuaj yeem yog tus neeg sawv cev kho mob rau lub raum puas los ntawm hypercholesterolemia [82]. Tsis tas li ntawd, N. Sativa ethanol extract kho elevated nitric oxide (NO) ntau ntau thiab lojraumarteriole txoj kab uas hla ntawm pre-eclampsia nas qauv [83]. N. Sativa thiab nws cov Cheebtsam kuj tau cog lus los tiv thaiv thiab kho nephrolithiasis thiab raum puas tsuaj [84].



4.2. Cov ntaub ntawv pov thawj ntawm kev tiv thaiv raum los ntawm Black Cumin

Dub cumintau qhia txog kev txhim kho ntawm cov kab mob tshwm sim hauv cov neeg mob CKD raws li qhia hauv ntau qhov kev tshawb fawb tib neeg. Kev tshuaj xyuas cov txheej txheem tsis ntev los no thiab kev tshuaj ntsuam meta-kev soj ntsuam ntawm randomized-tswj kev sim qhia tau hais tiasdub cuminntxiv rau hauv kev cuam tshuam mus sij hawm ntev thiab kev noj tshuaj txhua hnub tuaj yeem txo qhov tsis zoo ntawmraummuaj nuj nqi, suav nrog BUN [85]. Nyob rau hauv ib tug yav tom ntej, sib piv, thiab qhib-labeled txoj kev tshawb no rau cov neeg mob nrog CKD theem 3 thiab 4 ntawm ib tug tertiary care center nyob rau hauv North India, kev kho mob ntawm NSO (2.5 mL, po, ib zaug ib hnub rau 12 lub lis piam) qhov tseem ceeb kev kho mob nta thiab biochemical tsis. , suav nrog kev txo qis hauv cov ntshav urea, ntshav creatinine, thiab tag nrho cov zis protein thiab nce ntxiv ntawm cov zis ntim thiab glomerular filtration rate hauv 24 teev [27]. Lwm qhov kev tshawb fawb zoo sib xws tau qhia txog kev ua tau zoo thiab kev nyab xeeb ntawm NSO kev tswj hwm hauv cov neeg mob CKD theem 3 thiab 4 vim yog ntshav qab zib nephropathy. Muaj qhov txo qis hauv cov ntshav qabzib, cov ntshav creatinine, ntshav urea, thiab 24 teev tag nrho cov zis protein ntau thiab qhov nce ntxiv ntawm glomerular filtration rate, 24 teev tag nrho cov zis ntim, thiab qib hemoglobin hauv pab pawg kho mob.dub cuminyog'i [25]. Hauv ob qho kev tshawb fawb, cov kws sau ntawv qhia tias cov roj cumin dub tuaj yeem yog ib qho kev kho mob ntxiv uas tuaj yeem txhawb txoj kev kho kom zoo ntawm kev tswj xyuas cov neeg mob ntshav qab zib nephropathy. Kev tiv thaiv nephrolithiasis raws li qhia nyob rau hauv ib tug preclinical txoj kev tshawb no [71] tau muab txhais ntxiv mus rau ib tug randomized, triple-dig muag, placebo-tswj, soj ntsuam kuaj nyob rau hauv uas ob pab pawg neeg ntawm cov neeg mob (txhua tus nrog 30) nrog rau lub raum pob zeb tau txais ob lub noob dub tshuaj ntsiav (500). mg) lossis placebo ob zaug ib hnub rau 10 lub lis piam. Hauv pawg noob dub, 44.4 feem pua ​​​​ntawm cov neeg mob tau tso lawv cov pob zeb kom tiav, thiab qhov loj ntawm cov pob zeb tseem tsis hloov pauv thiab txo qis hauv 3.7 feem pua ​​​​thiab 51.8 feem pua ​​​​ntawm cov neeg mob, raws li, thaum nyob rau hauv cov placebo pab pawg, 15.3 feem pua ​​​​ntawm cov neeg mob tso lawv cov pob zeb. tag nrho, 11.5 feem pua ​​​​tau txo cov pob zeb loj, 15.3 feem pua ​​​​tau nce pob zeb loj, thiab 57.6 feem pua ​​​​tsis muaj qhov hloov pauv ntawm lawv cov pob zeb loj. Muaj qhov sib txawv tseem ceeb ntawm qhov loj me ntawm lub raum pob zeb ntawm ob pawg. Piv rau cov placebo, cov noob dub muaj cov txiaj ntsig zoo ntawm qhov ploj lossis txo qhov loj ntawmraumpob zeb [26].

Table 1. Summary on the protective effects of black cumin and TQ against various experimental kidney injury models.

AKI, Acute kidney injury; ALP, Alkaline phosphatase; ALT, Alanine aminotransferase; AMP, Activated protein kinase; AST, Aspartate aminotransferase; ATP, Adenosine triphosphate, As, Arsenic; BBM, Brush border membrane; BBMV, Brush border membrane vesicle; BIL, Bilirubin; BUN, Blood urea nitrogen; Bcl-2, B-cell lymphoma 2; CAT, Catalase; CCl4, Carbon tetrachloride; CKD, Chronic kidney disease; CP, Cisplatin; Cd, Cadmium; FENa, Fractional excretion of sodium; GFR, Growth factor receptor; GGTase, Geranylgeranyltransferase; GPx, Glutathione peroxidase; GSH, Glutathione; IRI–Ischemia-reperfusion injury; JNK, c-Jun N-terminal kinases; KIM-1, Kidney injury molecule- 1; LAP, latency-associated peptide; MDA, Malondialdehyde; NF-κB, Nuclear factor kappa B; NGAL, Neutrophil gelatinase-associated lipocalin; NSO, N. sativa oil; NSP, N. sativa seed powder; NSE, N. sativa seed extract; pJNK, Phosphorylated c-Jun N-terminal kinase; PAI-1, plasminogen activator inhibitor-1; RBF, Renal blood flow; SOD, Superoxide dismutase; TGF-β1, Transforming growth factor beta 1; TNF-α, Tumor necrosis factor alpha; TQ, Thymoquinone; α-SMA, Smooth muscle alpha-actin.

5. Teeb meem kev nyab xeeb

Dub cuminthiab nws cov bioactive Cheebtsam raug suav hais tias yog qhov ua tau zoo rau [86,87]. Txawm li cas los xij, TQ tuaj yeem, qee zaum, tsim oxidative kev nyuaj siab, cuam tshuam cellular macromolecules (DNA, lipids, thiab cov proteins) thiab cov kev taw qhia, xws li extracellular signal-regulated kinase (ERK), protein kinase C (PKC), thiab Ras, thaum. Lwm cov tshuaj bioactive los ntawm N. sativa tuaj yeem cuam tshuam nrog TQ-induced toxicity [88–90]. TQ toxicity yog, txawm li cas los xij, cov ntsiab lus-dependant.

Kev tswj hwm ntawm NSO txog li 2.5 mL (hais lus, ib zaug ib hnub) tau raug pov thawj tias muaj kev nyab xeeb ntawm biochemical thiab kev kho mob ntawm cov neeg mob ntshav qab zib nephropathy, tab sis ntau lwm cov kev tshawb fawb molecular yuav tsum tau lees paub cov lus [25]. Nws tseem muaj kev nyab xeeb los noj NSO (2.5 mL) peb zaug hauv ib hnub raws li kev kho ntxiv los txhim kho.raumkev ua haujlwm hauv cov neeg mob CKD [27]. Ib qho randomized, ob-dig muag, tshuaj placebo-tshuaj ntsuam xyuas nrog N. sativa pom qhov txo qis hauv lub raum pob zeb loj, txawm tias ib tug txiv neej ntawm 60 tus neeg mob muaj hydronephrosis thiab nce ntshav siab [26]. Txoj kev tshawb no muaj kev txwv xws li lub sij hawm luv luv thiab tsis muaj kev ntsuam xyuas tshwj xeeb (xws li tomography) uas tsim nyog los ntsuas qhov loj ntawm lub raum pob zeb [26].

Hauv ib daim ntawv tshaj tawm, NSE (100 mg / kg) tau siv ob lub lis piam tom qab noj CP, thiab tsis pom qhov tshwm sim ntawmraumbiochemical tsis tau pom nyob rau hauv nas [91]. Cov nas tau muab ntau koob tshuaj NSE (6, 9, 14, thiab 21 g / kg) thiab tsis muaj kev tuag [92]. Hauv lwm qhov kev sim, NSO supplementation (0.2, 0.4, {{10}}.4, 0.8, 1 mg/kg) rau nas thiab nas ua rau xoom kev tuag [93]. Txawm li cas los xij, muaj cov kev txwv hauv tus cwj pwm ntawm NSO thiab tsis muaj cov ntsiab lus uas tsis yog tag nrho cov kev ntsuam xyuas flavonoid. Ib daim ntawv tshaj tawm ntawm cov menyuam qaib broiler tau qhia tias kev ntxiv ntawm 20 thiab 100 g / kg N. Sativa noob rau 7 lub lis piam tsis muaj qhov cuam tshuam zoo rau biochemical / hematological profile, pathological nta, thiab kev loj hlob [94]. Cov kws tshawb fawb tau ua pov thawj tias qhov koob tshuaj ntau dua (25 mL / kg) ntawm NSO muaj cov tshuaj lom rau cov kev hloov pauv hauv lub raum cortex thiab qis dua (15 mL / kg) muaj qhov tsis zoo rau lub siab [95]. Tsis tas li ntawd, kev tshawb fawb yav dhau los tau pom tias TQ siab dua 10 mg / kg / hnub tsis pom muaj kev tiv thaiv tiv thaiv CP-induced nephrotoxicity [96]. Yog li ntawd, nws qhia tias cov koob tshuaj uas tsim nyog ntawm cov cumin dub lossis nws cov khoom yuav tsum tau ua kom tiav cov txiaj ntsig xav tau.

Table 2. Summary on the protective effects of black cumin against various kidney diseases in patients.

6. Cov lus xaus thiab cov kev xav yav tom ntej

Lub raumtas li raug rau ntau yam xenobiotics, xws li tshuaj, khoom noj khoom haus additives, tshuaj lom, thiab ib puag ncig chemicals. Qhov kev puas tsuaj ntawm cov xenobiotics no txwv nruj heevraumkev ua haujlwm thiab ua rau muaj kev loj hlob ntawm cov mob hnyav thiab cov kab mob raum ntev. Muaj qee qhov lwm yam tshwm sim, xws li ntshav qab zib, ntshav siab, dyslipidemia, thiab ischemia uas tseem ua rau muaj kev pheej hmoo ntawmraumkab mob. Ntau yam kev mob tshwm sim los ntawm cov kws kho mob uas twb muaj lawm txhawb cov kws tshawb fawb los tshawb nrhiav lwm txoj hauv kev nyab xeeb. Cov ntaub ntawv pov thawj los ntawm cov ntaub ntawv uas twb muaj lawm qhia tias raug xenobiotics, xws li tshuaj tua kab mob, cov hlau hnyav, tshuaj tua kab, thiab lwm yam tshuaj ib puag ncig ua rau lub raum raug mob hauv cov tsiaj sim, uas tau txhim kho los ntawm kev tswj hwm ntawm cumin dub thiab TQ (Daim duab 3). Ischemia / reperfusion tuaj yeem ua rau lub raum puas, uas tuaj yeem kho nrog cumin dub thiab TQ. Ntxiv mus, muaj ntau cov pov thawj tias dub cumin thiab TQ tuaj yeem txhim kho raum mob hauv kev sim ntshav qab zib thiab lwm yam teeb meem [97]. Cov txheej txheem plausible hauv qab kev tiv thaiv los ntawm dub cumin thiab TQ tiv thaiv ntau yam kab mob raum feem ntau koom nrog antioxidation, tiv thaiv kab mob, tiv thaiv apoptosis, thiab antifibrosis. Thaum cov ntaub ntawv pov thawj uas twb muaj lawm qhia tias NF-kB, Caspase, thiab TGF- kev taw qhia txoj hauv kev tau koom nrog hauv cov txheej txheem molecular ntawm dub cumin / TQ-mediated raum tiv thaiv teebmeem, nws yog ib qho tsim nyog los tshawb xyuas seb puas muaj lwm txoj hauv kev tseem ceeb xws li Nrf2 / HO{ {8}}, mTOR, MAPK yog cuam tshuam.

Cov txiaj ntsig ntawm kev kho mob tseem tau muab txhais ua cov kev kho mob raws li muaj pov thawj tias cov roj cumin dub tau muab rau cov neeg mob CKD siab heev normalizes hematological thiab urinary tsis thiab txhim kho cov txiaj ntsig ntawm cov kab mob. Txawm li cas los, nyob rau hauv thiaj li yuav pom zoo no natural tshuaj nyob rau hauv cov neeg mob nrograumCov teeb meem, kev tshawb fawb soj ntsuam ntxiv nrog rau tib neeg cov ntsiab lus tsim nyog, thiab ntev ntev yog lav. Cov ntaub ntawv ntawm nanoparticle-guided targeted xa hauv lub raum kuj tsis muaj. Txawm li cas los xij, qhov kev tshuaj xyuas no muab qee cov ntaub ntawv tseem ceeb uas cov kws tshawb fawb tuaj yeem siv los ua kev tshawb fawb yav tom ntej rau hauv cov tshuaj dub cumin / TQ-raws li kev kho mob raum kab mob.

Figure 3. Prospective kidney-protective effects of N. sativa and its active constituent. Bioactive compounds of N. sativa prevents kidney injury by inhibiting several stress stimuli induced apoptosis, oxidative stress, inflammation and fibrosis

1 ABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh; (MSZ);

2 Department of Biochemistry thiab Molecular Biology, Bangladesh Agricultural University, Mymensingh 2202, Bangladesh

3 Kawm tiav Tsev Kawm Ntawv Pharmaceutical Sciences, College of Pharmacy, Ewha Woman's University, Seoul 120-750, Kauslim;


Tus sau kev koom tes:Txoj haujlwm no yog kev sib koom tes ntawm txhua tus kws sau ntawv. MAH thiab MJU tsim cov qauv thiab sau cov ntawv sau. MSZ, PPS, thiab AM tau sau thawj tsab ntawv ntawm cov ntawv sau. MJU, AM, MAH, thiab HH tau tshuaj xyuas cov ntsiab lus tshawb fawb tau piav qhia hauv phau ntawv sau. Txhua tus kws sau ntawv tau nyeem thiab pom zoo rau qhov kawg xa tawm ntawm cov ntawv sau.

Nyiaj txiag:Txoj haujlwm no tau txais kev txhawb nqa los ntawm National Research Foundation (No. 2020R1I1A1A01072879) thiab Brain Pool program pab nyiaj los ntawm Ministry of Science thiab ICT los ntawm National Research Foundation (No. 2020H1D3A2A02110924), Republic of Korea.

Institutional Review Board Statement:Tsis siv tau.

Cov Lus Qhia Txog Kev Pom Zoo: Tsis siv tau.

Cov ntaub ntawv muaj nyob:Tsis siv tau.

Kev lees paub:MJU lees paub National Research Foundation (No. 2015H1D3A1062189), Republic of Korea.

Kev tsis sib haum xeeb ntawm kev txaus siab:Tsis muaj kev cuam tshuam ntawm kev txaus siab ntawm cov kws sau ntawv txog kev tshaj tawm cov ntawv sau no.

cistanche can prevent kidney infection symptoms and relieve chronic kidney disease

OrganicCov tshuaj cistanche tuaj yeem tiv thaiv lub raum raug mob thiab txo qismob raum mob, nyem qhov no kom taucov khoom


Cov ntaub ntawv

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