Abstract

Raws li kev tshawb fawb cuam tshuam,cistancheyog ib txwm suav tshuaj ntsuab uas tau siv rau ntau pua xyoo los kho ntau yam kab mob. Nws tau raug tshawb fawb pov thawj kom muajanti-inflammatory,anti-aging, thiabantioxidantkhoom. Cov kev tshawb fawb tau pom tias cistanche muaj txiaj ntsig zoo rau cov neeg mob uas muaj kab mob raum. Cov khoom xyaw nquag ntawm cistanche paub txogtxo qhov mob, txhim kho lub raum ua haujlwmthiabrestore lub raum puas hlwb. Yog li, kev sib koom ua ke cistanche hauv txoj kev npaj kho mob raum tuaj yeem muab txiaj ntsig zoo rau cov neeg mob hauv kev tswj hwm lawv tus mob. Cistanche pab txo qis proteinuria, txo qis BUN thiab creatinine qib, thiab txo qhov kev pheej hmoo ntawm lub raum puas. Tsis tas li ntawd, cistanche kuj pab txo cov roj cholesterol thiab triglyceride uas tuaj yeem ua rau muaj kev phom sij rau cov neeg mob uas muaj kab mob raum.

Nyem rau ntawm Cistanche Tubulosa Ntxiv

Yog xav paub ntxiv:

david.deng@wecistanche.com WhatApp:86 13632399501

Keeb kwm

Cov txheej txheem o yog koom nrog hauv lub cev tiv thaiv kab mob, uas tswj cov ntaub so ntswg homeostasis thaum lub sij hawm tsis zoo, xws li kis kab mob thiab lwm yam kev raug mob. Cov txheej txheem no ua rau txo qis ntawm cov ntaub so ntswg ua haujlwm thiab ua haujlwm los ntawm kev ua kom cov txheej txheem kho [1,2].

Mob, kub, liab, thiab o yog universal cov cim qhia uas nrog tag nrho cov txheej txheem inflammatory, uas tshwm sim los ntawm dilation ntawm venules thiab arterioles, txhim khu cov hlab ntsha permeability, ntshav txaus nrog percolation ntawm leukocytes rau hauv cov ntaub so ntswg, thiab tso tawm inflammatory mediators [3].

Keeb kwm, plaub lub cim tau cuam tshuam nrog qhov txhab thiab kab mob rau ntau txhiab xyoo, raws li tau piav qhia los ntawm tus kws kho mob Roman Cornelius Celsus nyob rau xyoo pua AD. Nyob rau hauv 1846 thiab 1867, Augustus Waller thiab Julius Cohnheim, raws li, tau piav qhia txog lub ntsiab yam ntxwv ntawm ib tug mob inflammatory txheej txheem los ntawm leukocyte emigration los ntawm cov hlab ntsha thiab vascular hloov. Lwm qhov tseem ceeb ua ntej hauv daim teb no yog Elie Metchnikoff, xyoo 1892, uas tau tshawb pom phagocytosis thiab lub luag haujlwm tseem ceeb ntawm macrophages thiab macrophages (neutrophils) hauv kev tiv thaiv tus tswv thiab kev saib xyuas cov ntaub so ntswg homeostasis. Lub tswv yim no yog lub tswv yim tam sim no hais tias mob inflammatory teb yog ib qho kev tiv thaiv thiab ciaj sia taus rau cov ntaub so ntswg [1,4].

Hauv cov ntsiab lus no, o tuaj yeem suav hais tias yog ib qho tseem ceeb hauv kev loj hlob ntawm cov kab mob pathological ntawm cov kab mob hnyav thiab mob ntev hauv lub raum. Cov yam ntxwv ua haujlwm ntawm lub cev no ua rau nws muaj peev xwm tsim tau ntau yam kev mob raum, xws li mob raum raug mob (AKI) thiab mob raum mob (CKD). Kev tshawb nrhiav kev txhais lus hauv cheeb tsam no yuav tsum xav txog ntau qhov kev tshawb pom ntawm cov kab mob ntawm cov txheej txheem inflammatory uas tshwm sim los ntawm kev tshawb fawb hauv chav kuaj - lub rooj ntev zaum - nqa cov kev tshawb pom muaj feem cuam tshuam uas tshwm sim los ntawm cov kab lis kev cai ntawm tes lossis kev sim tsiaj (hauv vitro lossis hauv vivo). Cov lus teb los ntawm lub rooj ntev zaum yuav tsum tau siv nyob rau hauv lub tsev kho mob xyaum - lub txaj txaj - nyob rau hauv ua ob qho tib si kev tshawb fawb soj ntsuam thiab soj ntsuam kev sim. Kev tshawb nrhiav kev txhais lus txhawb nqa lub zog ntawm ntau pawg kws tshawb fawb los ntawm kev qhia txog kev cawm neeg txoj sia rau cov kab mob sib txawv thiab kev xyaum ua pov thawj [5].

Cov txheej txheem

Cov txiaj ntsig thiab kev sib tham

Raws li cov txheej txheem xaiv, 689 cov kev tshawb fawb 'cov npe thiab cov lus piav qhia tau suav nrog hauv cov txheej txheem txheeb xyuas; 345 cov kev tshawb fawb raug tshem tawm, 287 cov kev tshawb fawb raug xaiv rau kev tshuaj xyuas tag nrho cov ntawv thiab 45 cov kev tshawb fawb tau suav nrog hauv kev tshuaj xyuas zaum kawg. PRISMA flowchart yog qhia hauv daim duab 1.

Inflammatory teb

1. Kev raug mob los yog kis tau los ntawm receptors ntawm lub cev tiv thaiv kab mob [1,6].

2. Kev pib ntawm cov lus teb inflammatory hauv lub cev, koom nrog cov tsev neeg tsis muaj kab mob los yog kis kab mob ntawm cov receptors qhia hauv cov ntaub so ntswg-cov neeg nyob hauv macrophages, dendritic cells, thiab mast cells [7].

3. Kev tsim cov inflammatory cytokines, chemokines, bioactive amines, eicosanoids, thiab bradykinin uas txhim khu cov hlab ntsha permeability induced vasodilatation ntawm venules thiab arterioles nrog rau migration ntawm leukocytes rau hauv cov ntaub so ntswg [3,8].

4. Infiltration ntawm leukocytes, uas ua si ib tug loj tiv thaiv teb nyob rau hauv cov ntaub so ntswg raug mob los ntawm neutralizing thiab tshem tawm tej yam uas yuav raug mob stimuli aiming los daws qhov mob inflammatory teb. Cov ntaub so ntswg mus rau kev daws teeb meem los ntawm kev rov qab los ntawm homeostasis thiab tshem tawm cov hlwb tuag [9].

Oxidative stress thiab inflammatory teb

Cov txheej txheem o thiab oxidative kev nyuaj siab yog cov xwm txheej pathophysiological uas txuas rau ib leeg. Raws li qhov xwm txheej ntawm lub cev, cov cellular metabolism hauv ib txwm ua rau cov pa oxygen reactive (ROS) thiab cov kab mob nitrogen reactive (RNS) uas tau raug tshem tawm zoo nyob rau hauv muaj cov tshuaj tiv thaiv antioxidant [10,11]. Yog li, inflammatory cells tsim ntau ROS thiab RNS uas pib intracellular signaling cascading thiab txhim kho proinflammatory gene qhia [6,8].

Kev tsim tawm ntau dhau ntawm ROS thiab RNS tuaj yeem hloov kho qhov sib npaug ntawm qhov sib npaug ntawm oxidative kev nyuaj siab, thiab ua lub luag haujlwm tseem ceeb hauv cov ntaub so ntswg raug mob [10,11]. Oxidative kev nyuaj siab yog tshwm sim los ntawm kev tsim cov kab mob ntau ntxiv, xws li nitric oxide (NO) thiab hydrogen peroxide (H2 O2), thiab muaj zog oxidants, xws li superoxide anions (O2 •-) thiab hydroxyl radical (OH•-). ROS thiab RNS deplete thiab txo qhov muaj peev xwm antioxidant, thiab tuaj yeem ua rau raug mob hauv txhua qhov tseem ceeb ntawm tes los ntawm oxidation ntawm cov protein, peroxidation ntawm lipids, thiab DNA puas, ua rau cell tuag [12]. Cov ntaub ntawv pov thawj los ntawm kev sim cov ntaub ntawv tau pom tias muaj kev sib koom ua ke ntawm inflammatory teb thiab oxidative kev nyuaj siab nyob rau hauv ntau yam kab mob [13].

Mob o thiab mob ntev

Cov txheej txheem inflammatory yog ib qho kev sib koom tes teb los ntawm kev ua kom cov kab mob ntawm tes thiab tso tawm cov inflammatory mediators uas ua rau cov ntaub so ntswg raug mob. Kev mob yog ib qho nyuaj ntawm lub cev teb rau cov kab mob txawv teb chaws, suav nrog tib neeg cov kab mob thiab ntau yam kab mob thiab kab mob. Cov kab mob tau muab faib ua mob hnyav thiab mob ntev, nyob ntawm ntau yam txheej txheem inflammatory thiab cellular mechanisms. Nws tau raug suav hais tias yog qhov tseem ceeb rau kev loj hlob ntawm ntau yam kab mob / kab mob, suav nrog ntshav qab zib, mob qog noj ntshav, kab mob plawv, kab mob hauv lub raum, mob qhov muag, mob caj dab, rog rog, kab mob autoimmune, thiab kab mob plab hnyuv. Kev tsim tawm dawb radical los ntawm cov khoom siv roj ntsha thiab ib puag ncig thiab nws qhov tsis sib xws nrog cov tshuaj antioxidants ntuj ntxiv ua rau ntau yam kab mob sib kis [6, 7].

Kev mob hnyav yog ib qho kev tiv thaiv kab mob luv luv thiab kev txwv tus kheej, kav ntev li ntawm feeb mus rau ob peb hnub. Lub cev tiv thaiv kab mob ua kom muaj cov kab mob sib kis, txhim kho microvascular permeability, tso tawm ntawm cov plasma proteins los yog kua dej, thiab txav ntawm leukocytes mus rau hauv lub extravascular cheeb tsam, yam ntxwv ntawm classic cov cim ntawm tshav kub, liab, thiab o. Tsis tas li ntawd, inflammatory mediators nce rhiab heev ntawm cov ntaub so ntswg rau qhov mob [9,14].

Lub ntsiab feature ntawm inflammatory mediators yog lub luv luv ib nrab-lub neej thaum lub raug mob stimulus raug tshem tawm thiab yog li mob inflammatory ntsiab, nyob rau hauv ib tug active txheej txheem, uas ua rau biosynthesis ntawm active mediators - pro- daws cov neeg kho kom haum xeeb - uas ua los txhawb cov ntaub so ntswg homeostasis [8, 15, 16, 17] ib. Cov teebmeem ntawm cov lus teb ntev ntev yog cuam tshuam nrog kev kho mob tsis tu ncua thiab tuaj yeem raug mob los ntawm kev raug mob tsis tu ncua, kis kab mob, los yog ntev raug rau cov tshuaj lom neeg, ua rau mob ntev, cov ntaub so ntswg puas, fibrosis, thiab necrosis.

Qhov mob ntawm cov nqaij mos no tau cuam tshuam nrog ntau qhov tshwm sim los ntawm cov lus teb lom neeg nrog kev txhim kho kev pheej hmoo ntawm cov kab mob thiab cov kab mob tsis zoo [18,19].

Kev mob hnyav yog ib qho kev tiv thaiv kev noj qab haus huv, uas muaj cov txheej txheem ntawm cov cellular thiab molecular xwm txheej uas txo cov kev raug mob los yog kis kab mob [1]. Kev mob o tuaj yeem tiv thaiv, tab sis qhov mob tsis tswj tau tuaj yeem ua rau cov ntaub so ntswg puas, ua rau cov kab mob ntev. Tam sim no, o tuaj yeem suav hais tias yog ib qho tseem ceeb hauv kev ua haujlwm ntawm cov kab mob hnyav thiab mob ntev hauv cov kab mob sib txawv, xws li lub plawv, pancreas, siab, raum, ntsws, hlwb, plab hnyuv, thiab lub cev xeeb tub. Cov txheej txheem no nyob ntawm qhov xwm txheej ntawm etiology stimulus thiab nws qhov chaw nyob hauv lub cev [20].

Cov ntaub ntawv pov thawj rau kev tswj tsis tau tus mob yog ib qho tseem ceeb rau ntau yam kab mob, nrog rau cov kab mob plawv, kab mob plab hnyuv, kab mob neurodegenerative xws li Alzheimer's thiab Parkinson's, hawb pob, mob qog noj ntshav, ntshav qab zib, thiab kab mob autoimmune [18,21].

Lub raum

Physiologically thiab metabolically, lub raum yog cov feem ntau nyuaj hauv lub cev. Lub raum yog lub luag haujlwm tseem ceeb hauv lub cev uas tuaj yeem ua kom tshem tawm cov khoom pov tseg los ntawm cov metabolism, kev saib xyuas dej thiab electrolyte homeostasis, thiab endocrine functions. Cov kev ua haujlwm ntawm lub raum yog cov nephrons, muaj cov glomerulus (cov hlwb endothelial) thiab cov tubule ntev (cov hlwb epithelium). Lub raum yog perfused nrog 20 mus rau 25 feem pua ​​​​ntawm cov zis tawm mus rau 125 mL / feeb ntawm cov lim kom dhau mus rau Bowman capsule uas yog reabsorbed los ntawm peritubular capillary network thiab tsim tawm txog 1.5 L ntawm cov zis txhua hnub. Cov yam ntxwv ua haujlwm ntawm lub cev no ua rau muaj qhov tsis zoo rau kev tsim ntau hom kev raug mob raum - AKI thiab CKD [22].

AKI txhais tau tias yog qhov txo qis hauv lub raum ua haujlwm, uas tshwm sim los ntawm ntau qhov kev thuam hauv glomerulus - tom qab kis kab mob glomerulonephritis, lupus nephritis, IgA glomerulonephritis - hauv tubule - lub raum ischemia (poob siab, phais, hemorrhage, raug mob, kab mob pancreatitis), cev xeeb tub, mob pancreatitis. nephrotoxic tshuaj (cov tshuaj tua kab mob, tshuaj antineoplastic, sib piv media, organic solvents, tshuaj loog, hnyav hlau) thiab endogenous co toxins (myoglobin, hemoglobin, uric acid) [23]. Feem ntau ntawm AKI txawv ntawm 1 mus rau 25 feem pua ​​​​thiab kev tuag ntawm 15 mus rau 60 feem pua, thiab qhov ntawd nce mus txog 50 mus rau 60 feem pua ​​​​hauv cov neeg mob hauv cov tsev kho mob hnyav [23,24].

Kev mob tshwm sim ua lub luag haujlwm tseem ceeb hauv pathophysiology ntawm AKI. Nyob rau hauv lub raum, qhov mob inflammatory teb ua rau txhim kho endothelial cell-leukocyte adhesion uas cuam tshuam cov ntshav khiav hauv lub raum microvasculature. Leukocytes tuaj yeem qhib los ntawm cov kws kho mob inflammatory, xws li cytokines, ROS, RNS, thiab eicosanoids. Hauv kev teb rau qhov mob, lub raum tubule epithelium hlwb kuj tsim cov neeg kho kom haum xeeb uas muaj peev xwm ua rau lub cev ntawm qhov mob [25].

Kev sim kev tshawb fawb ntawm AKI - ischemia thiab reperfusion qauv, sepsis-endotoxemia qauv, thiab nephrotoxic qauv - tau pom cov leukocytes, suav nrog neutrophils, macrophages, ntuj killer cells, thiab lymphocytes infiltrating rau hauv qhov chaw raug mob, uas ua rau muaj kev hloov pauv hauv vascular endothelial hlwb lossis tubular epithelium hlwb [3,26].

Lub raum endothelial hlwb, tubular epithelium hlwb, thiab inflammatory hlwb nyob rau hauv complex cross-hais lus perpetuate up-regulated ntawm cytokines thiab chemokines, ROS thiab RNS, thiab vasoconstrictors - prostaglandins, leukotrienes, thiab thromboxane - uas ua rau infiltration ntawm inflammatory hlwb mus rau hauv lub raum. ntaub so ntswg. Cov txheej txheem no tuaj yeem txiav txim siab ntxiv los yog txo cov txheej txheem o hauv lub raum los ntawm kev tsim cov pro-inflammatory lossis anti-inflammatory cytokines [3,26,27].

Cov kab mob rhiab heev hauv cov ntaub so ntswg teb los ntawm kev raug mob lossis kev kis kab mob yog cov lus teb lom neeg nrog rau ntau qhov kev tshwm sim thib ob uas txhim kho kev pheej hmoo ntawm cov kab mob ntev. Cov txheej txheem inflammatory tsis tu ncua ua rau muaj kev cuam tshuam tsis zoo rau cov ntaub so ntswg ua haujlwm lossis cov ntaub so ntswg puas. Tsis tas li ntawd, cov kab mob inflammatory ua rau cov kab mob dysregulated kho cov ntaub so ntswg, nrog rau cov ntaub so ntswg remodeling, fibrosis, thiab cov nqaij mos metaplasia. Lub dysregulation ntawm o yog zoo ib yam li cov ntaub so ntswg pathology los yog poob rau hauv cov ntaub so ntswg function [1].

Cov txheej txheem molecular thiab cellular ntawm cov kab mob sib kis sib txawv thiab nyob ntawm seb hom kab mob thiab cov kab mob hauv nruab nrog cev [28]. Qhov kev loj hlob ntawm CKD yog aggravated los ntawm cov kab mob inflammatory teb. Cov txheej txheem no ua rau glomerular o, uas ua rau cov proteinuria vim kev puas tsuaj rau glomerular capillaries. Tubule raug mob tuaj yeem ua rau fibrosis hauv lub raum cov ntaub so ntswg [29,30]. Tsis tas li ntawd, oxidative kev nyuaj siab los ntawm depletion ntawm endogenous intracellular antioxidant pab txhawb azotemia, siab glomerular thiab tubular raug mob, thiab nce qib ntawm inflammatory mediators. Ob leeg mob ntev thiab oxidation ntawm lub raum hlwb txo glomerular pom, uas ua rau lub raum puas tsuaj thiab tsis ua haujlwm [31].

CKD kuj tau piav qhia los ntawm kev txo qis glomerular filtration rate (GFR) thiab tshem tawm cytokines, txhim kho qib ntawm cov cytokines thiab pro-oxidative metabolites. Cov txiaj ntsig ntawm CKD cov neeg mob tuaj yeem cuam tshuam nrog nce qib ntawm cov kua dej nitrogenous pov tseg, metabolic acidosis, thiab nquag kis kab mob [33].

Kev mob thiab kev tiv thaiv kab mob hauv cov neeg mob CKD tuaj yeem ua tau los ntawm kev kho hemodialysis. Cov txheej txheem extracorporeal ua rau cov txheej txheem inflammatory cytokines los ntawm impurities hauv dej lim dej, microbiological zoo ntawm dialysate, thiab bio-incompatible yam hauv lub extracorporeal dialysis circuit [34,35]. Tsis tas li ntawd, cov neeg mob ntshav lim ntshav tuaj yeem cuam tshuam nrog cov xwm txheej sib kis thiab cov kab mob thrombotic uas ua rau muaj kev mob tshwm sim. Cov xwm txheej no suav nrog cov kab mob ntsig txog kab mob hauv cov hlab ntshav, nkag mus rau qhov chaw kis kab mob, thrombosed intravascular fistulae thiab grafts, thiab ntu ntawm peritonitis hauv cov neeg mob peritoneal dialysis [36].

Cov kab mob raum biomarkers

Cov txheej txheem kuaj mob tsis ntev los no yog npaj los ntawm Kab Mob Raum: Txhim Kho Ntiaj Teb Cov Txheej Txheem (KDIGO) cov lus qhia, uas piav qhia txog AKI raws li kev hloov pauv hauv cov ntshav creatinine (SCr) thiab cov zis tso zis (UO). AKI yog txhais los ntawm kev nce qib ntawm SCr mus rau tsawg kawg yog {{0}}.3 mg/dL lossis ntau dua 1.5 npaug ntawm qhov pib hauv 48 teev, lossis UO txo qis dua 0.5 mL/kg/ h rau 6h. KDIGO cov txheej txheem stratify peb theem ntawm AKI (Table 1) [37].

CKD yog txhais los ntawm GFR txo qis dua 60mL / min / 1.73m² rau ntau tshaj peb lub hlis lossis lub raum puas los ntawm albuminuria rau ntau tshaj peb lub hlis. Txawm hais tias nce tso zis albumin tawm thiab SCR qib, nrog rau qhov txo qis GFR, kuj yog cov cim tseem ceeb ntawm lub raum tsis ua haujlwm [38].

CKD tau muab faib ua theem ntawm qhov hnyav rau kev kuaj mob thiab tswj tus kab mob (Table 2) [38].

Tam sim no, cov txheej txheem kuaj mob ntawm lub raum yog raws li kev hloov pauv ntawm SCr thiab UO, qhov twg AKI tau txhais los ntawm kev nce SCr thiab txo UO. CKD raug kuaj pom los ntawm kev ntsuas lub raum puas los ntawm albuminuria thiab txo GFR [23]. Yog li, SCr thiab UO yog cov cim uas tau siv rau hauv kev kho mob.

SCr muaj qhov tsis zoo nyob rau hauv qhov chaw ntawm lub raum raug mob. Cov cim no tsis zoo vim tias nws raug cuam tshuam los ntawm ntau yam xws li hnub nyoog, poj niam txiv neej, cov leeg nqaij, kev tswj xyuas dej, thiab kev tso tawm ntawm qee yam tshuaj. Ntawm qhov tod tes, UO yog qhov cim ntxov rau lub raum tsis ua haujlwm uas tuaj yeem cuam tshuam los ntawm tus neeg mob lub cev thiab hemodynamic xwm txheej lossis kev tswj hwm cov tshuaj diuretics, yog li nws nyuaj rau ntsuas UO yam tsis muaj lub tso zis tso zis [39,40].

Qhov zoo tshaj plaws biomarker tuaj yeem kwv yees thiab kuaj xyuas ntau hom thiab etiology ntawm kab mob raum lossis qhov chaw ntawm qhov raug mob. Kev siv cov qauv tsis cuam tshuam thiab nkag tau yooj yim muab cov txiaj ntsig sai, kwv yees cov txiaj ntsig tau, thiab ua rau pib thiab saib xyuas cov kev pabcuam kho mob. Ntau yam molecules tau raug txheeb xyuas nyob rau hauv cov kab mob hauv lub cev thiab glomerular filtration markers ntawm glomerular muaj nuj nqi, xws li enzymes uas tso tawm los ntawm tubular hlwb mus rau hauv cov zis tom qab tubular cell raug mob, piav raws li cov cim ntawm tubular puas, los yog inflammatory mediators tso tawm los ntawm lub raum hlwb los yog infiltrating. inflammatory hlwb, piav raws li cov cim ntawm kev puas tsuaj thiab cov cim qhia ntawm qhov chaw ntawm kev raug mob [41,42].

Kev siv lub tswv yim "los ntawm lub rooj zaum mus rau txaj" hauv vivo lossis hauv vitro kev tshawb fawb tau ua rau muaj kev cog lus rau lub raum biomarkers los ntawm cov molecules uas qhia txog glomerular filtration thiab tubule raug mob, thiab tsis yog lub raum biomarkers tau los ntawm cov molecules uas tau lim, secreted, los yog reabsorbed. , molecules uas yog constitutive los yog upregulated los yog molecules ntawm lub cev tiv thaiv kab mob infiltration [41]. Txawm hais tias qee qhov inflammatory molecules los ntawm cov kev tshawb fawb yooj yim tuaj yeem yog biomarker muaj txiaj ntsig rau kev tshawb nrhiav thiab kuaj mob raum, cov biomarkers uas sawv tawm hauv cov ntsiab lus no yog cov neutrophil gelatinase-associated lipocalin (NGAL), raum raug mob molecule-1 (KIM -1) thiab interleukin 18 (IL-18).

Neutrophil gelatinase-associated lipocalin

Neutrophil gelatinase-associated lipocalin (NGAL) yog cov protein txuam nrog gelatinase los ntawm neutrophils [43,44]. Nyob rau hauv lub cev lub cev, NGAL protein ntau muaj tsawg heev nyob rau hauv ntau yam kua lom lom. Nws raug tso tawm los ntawm daim siab, spleen, thiab ob lub raum [45]. NGAL yog upregulated thiab tso tawm mus rau hauv cov zis thiab plasma nyob rau hauv lub cellular raug mob. Vim tias NGAL yog qhov hnyav molecular uas tsis muaj qhov hnyav thiab tus nqi zoo uas dhau mus rau glomerular pom, lim NGAL raug tshem tawm los ntawm endocytosis los ntawm apical membrane thiab nws tshwm sim hauv cov zis [46].

Ntau qhov kev tshawb fawb pom tau hais tias cov neeg mob uas muaj qib siab ntawm NGAL yam tsis tau nce SCr tau muaj kev pheej hmoo tuag ntau dua li cov neeg mob siab SCr ib leeg [47]. Kev tshawb pom ntxov ntawm NGAL kuj tau piav qhia tias cov zis NGAL raug cais tawm ntawm cov neeg mob uas tsim AKI los ntawm cov neeg mob uas tsis nyob hauv tsev kho mob cirrhotic cov neeg mob [48], thiab nce qib ntshav NGAL tau cuam tshuam nrog kev pheej hmoo ntawm kev tsim AKI hauv cov neeg mob plawv tsis ua hauj lwm mob plawv [ 49] ib.

Lub raum raug mob molecule-1

Lub raum raug mob molecule-1 (KIM-1) yog tsim los ntawm cov tubular ze ze tom qab ischemic lossis nephrotoxic raug mob, thiab nws cov qib mRNA nce ntau dua li lwm cov noob tom qab raug mob raum [50].

Kev nthuav dav KIM-1 tau pom nyob rau hauv cov kab mob sib kis ntawm tubule epithelial nyob rau hauv tib neeg lub raum biopsy seem los ntawm cov neeg mob uas mob tubular necrosis [51]. Folic acid thiab cisplatin nephrotoxic qauv ntawm AKI pom tau hais tias qhov upregulation ntawm KIM-1 qhia ua ntej qhov nce ntawm SCr thiab ua hauj lwm raws li ib tug dav biomarker rau tubular raug mob [52]. Tsis tas li ntawd, urinary KIM-1 qib tau nce siab dua hauv cov neeg mob uas muaj ischemic AKI piv rau cov neeg mob uas muaj lwm yam etiologies ntawm AKI [53]. KIM-1 tau piav qhia tias yog ib qho tseem ceeb kwv yees ntawm AKI hauv ntau qhov xwm txheej ntawm kev kho mob - hauv cov neeg mob tom qab phais plawv thiab cov neeg mob hnyav thiab, KIM-1 qhov siab tau tshwm sim nyob rau hauv cov sij hawm ntawm lub raum raug mob [54, 55] ib.

Cov kev tshawb fawb soj ntsuam thawj zaug tau qhia tias nce urinary KIM-1 qib yog cov biomarker tshiab, thiab KIM-1 tau pom zoo los ntawm United States Food and Drug Administration ua biomarker rau kev kho tshuaj kho mob [41].

Interleukin 18

Interleukin 18 (IL-18) yog ib tug tswv cuab ntawm interleukin -1 cytokine superfamily thiab hu ua interferon- -inducing yam uas tswj innate thiab adaptive tiv thaiv teb [56]. Cov cytokine no yog tsim los ntawm cov hlwb mononuclear, macrophages, thiab cov hlwb tsis muaj zog nrog rau cov cell tubule. IL-18 kev ua haujlwm tau piav qhia hauv ntau yam kab mob, xws li mob caj dab, ntau yam sclerosis, kab mob plab hnyuv, kab mob siab ntev, kab mob lupus erythematosus, thiab psoriasis [56]. Upregulated qhia ntawm lub raum IL-18 tau pom nyob rau hauv ischemia-reperfusion raug mob, inflammatory nephritis, thiab cisplatin-induced nephrotoxicity [57].

Cov zis IL-18 qib tau nce ntxiv hauv cov neeg mob uas muaj mob qog nqaij hlav hauv plab piv rau prerenal azotemia, urinary tract infection, CKD, thiab nephrotic syndrome [58]. thiab, nyob rau theem siab dua ntawm IL-18 yog qhov cim ntxov ntawm AKI thiab qhov kev kwv yees zoo ntawm kev tuag hauv cov neeg mob hnyav [59]. Tsis tas li, kev tshuaj xyuas thiab kev tshawb xyuas meta-analysis tau piav qhia tias cov zis IL-18 yuav muaj txiaj ntsig zoo rau kev kwv yees kev txhim kho ntawm AKI [60].

Kev cog lus biomarkers ntawm cov kab mob raum

Ntau lub biomarkers tau siv rau kev kuaj mob ntxov ntxov ntawm cov kab mob raum hauv cov qauv tsiaj lossis cov chaw kho mob tshwj xeeb, ua kom pom lub peev xwm los txhim kho cov neeg mob. Lub raum cov ntaub so ntswg yog heterogeneous, thiab tam sim no, cov txheej txheem tsom mus rau thaj chaw tshwj xeeb ntawm nephron thiab sawv cev rau cov txheej txheem sib txawv ntawm cov kab mob raum teb hauv cov txheej txheem ntawm lub raum raug mob [61].

IB -6

IL-6 yog tus neeg nruab nrab uas muaj kev cuam tshuam. Kev ua rau lub raum tsis zoo cuam tshuam nrog cov lus teb inflammatory, thiab IL-6 yog ib qho inflammatory marker nyob rau hauv cov neeg mob lub raum, ua rau lub cev inflammatory marker C-reactive protein. Nce ntshav los yog zis IL-6 qib yog qhov cim ntxov ntawm kab mob raum [61].

Soluble TNF receptors

Soluble TNF receptors (TNFR1 thiab TNFR2) yog circulating biomarkers ntawm o. TNF receptors ua lub luag haujlwm tseem ceeb hauv kev txhim kho ntawm atherosclerotic thiab raum kab mob thiab cuam tshuam nrog kev mob ntshav qab zib nephropathy mus rau CKD theem 3 thiab kab mob raum kawg [62].

5-methoxy tryptophan

5-methoxy tryptophan (5-MTP) yog ib qho endogenous tryptophan metabolite thiab hloov los ntawm tryptophan hydroxylase-1 enzyme. 5-MTP muaj cov haujlwm tiv thaiv kab mob. Chen et al tau ua pov thawj tias tryptophan tau pom zoo ib yam nrog 5-MTP hauv cov neeg mob CKD, ntshav qab zib 5-MTP qib qis nrog kev nce qib ntawm CKD, thiab kev kho mob ntawm 5-MTH hauv unilateral ureteral obstruction tsiaj qauv attenuated raum interstitial fibrosis los ntawm kev txo cov inflammatory signaling molecules [63].

Cov roj ntsha

Lub raum ua haujlwm tuaj yeem cuam tshuam rau qib ntshav thiab tso zis tawm ntawm cov metabolites. Yog li, kev hloov pauv hauv lipid metabolism tuaj yeem ua rau muaj kev loj hlob ntawm CKD. Cov kab mob lipid ua kom nrawm atherosclerosis thiab kab mob plawv hauv cov neeg mob CKD [20, 33].

Feng thiab cov npoj yaig tau piav qhia tias fatty acid metabolism tau cuam tshuam nrog kev hloov pauv albuminuria, txo qis polyunsaturated fatty acids - docosahexaenoic acid (DHA), docosatrienoic acid (DTA), thiab cov peev xwm hloov pauv hloov pauv (TTA) - thiab nce saturated fatty acids (SFA), xws li raws li 5,8-octadecadienoic acid (5,8-TDA) thiab eicosadienoic acid (EDA) hauv CKD cov neeg mob uas muaj microalbuminuria thiab macroalbuminuria [64].

Cov lus xaus

Cov ntawv luv

Muaj cov ntaub ntawv thiab cov ntaub ntawv

Nyiaj txiag

Kev nyiam sib tw

Cov neeg sau ntawv pab txhawb

Kev pom zoo ntawm Ethics

Tso cai rau kev tshaj tawm

Cov ntaub ntawv

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