mwwXaiv lus
Tsev / Kev paub / Ntsiab lus

Kev paub

Ntu Ⅰ Catalytic Antioxidants nyob rau hauv lub raum

Apr 19, 2023

Abstract

Reactive oxygen thiab reactive nitrogen yog cuam tshuam nrog rau lub raum raug mob, nrog rau mob raum raug mob, mob raum kab mob, hypertensive nephropathy, thiab ntshav qab zib nephropathy. Yog li ntawd, antioxidants yog ib qho tseem ceeb hauv kev kho mob raum kab mob. Catalytic antioxidants tau txhais tias yog me me molecule mimics ntawm antioxidant enzymes xws li superoxide dismutase, catalase, thiab glutathione peroxidase, qee qhov uas muaj zog detoxifiers ntawm lipid peroxides thiab peroxynitrite. Ntau cov catalytic antioxidants tau pom tias muaj txiaj ntsig zoo hauv ntau yam hauv vitro thiab hauv vivo kab mob qauv cuam tshuam nrog oxidative kev nyuaj siab, suav nrog kab mob raum. Kab lus no tshuaj xyuas lub luag haujlwm ntawm cov enzymes antioxidant hauv lub raum kab mob, kev faib cov catalytic antioxidants, thiab lawv cov kev siv tam sim no hauv lub raum kab mob.

Ntsiab lus

catalase; glutathione peroxidase; superoxide dismutase; catalytic antioxidants; raum;Cov txiaj ntsig Cistanche.

Cistanche benefits

Nyem qhov no kom tau txaisCistanche cuam tshuam rau lub raum

Taw qhia

Oxidative stress piav txog qhov tsis sib xws ntawm kev tsim cov tshuaj reactive thiab kev tiv thaiv ntawm antioxidants thaum redox signaling los yog molecular puas tsuaj. Reactive oxygen hom (ROS) thiab reactive nitrogen hom (RNS) yog tshuaj lom los ntawm cov khoom tseem ceeb ntawm cov pa metabolism hauv cov kab mob nyob. Cov dawb radicals no suav nrog superoxide (O2-), hydrogen peroxide (H2O2), nitric oxide (NO-), hydroxyl radicals (OH-), peroxynitrite (ONOO-), thiab lipid peroxyl radicals (LOO-). Thaum ua pa, intracellular O2- yog tsim endogenously nyob rau hauv mitochondria, thiab ROS yog tsim los ntawm complexes nyob rau hauv lub electron thauj saw thiab los ntawm ib feem txo cov metabolites ntawm molecular oxygen tsim nyob rau hauv cov kab mob lom. Ntau ROS ntau lawm tshwm sim los ntawm kev ua kom cov oxidative enzymes tshwj xeeb, suav nrog nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), xanthine oxidase, uncoupled nitric oxide synthase (NOS), thiab arachidonic acid metabolizing enzymes.ROS induces protein ntau puas. , carbohydrates, thiab DNA, thaum kawg ua rau lub cev tsis ua haujlwm. Yog li ntawd, lawv tau raug suav hais tias yog cov tswj hwm tseem ceeb hauv ntau txoj hauv kev ntawm cov xov tooj ntawm tes txij li thaum ntxov (Daim duab 1). Antioxidant tiv thaiv mechanisms yog complex thiab compartmentalized thiab nws tus kheej tswj ROS theem nyob rau hauv lub cytoplasm, mitochondria, thiab nucleus. Hauv kev ua neej nyob, ROS qib yog tswj hwm los ntawm ntau yam antioxidant enzymes, suav nrog superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxiredoxin (Prx), thioredoxin (Trx), thiab cytochrome c oxidase.

Figure 1

Daim duab 1. Schematic txheej txheem cej luam ntawm endogenous qhov chaw ntawm oxidative kev nyuaj siab thiab antioxidative tshuaj tiv thaiv nyob rau hauv lub raum puas. Exogenous (ib puag ncig tej yam xws li huab cua thiab dej paug, haus luam yeeb, tshuaj, thiab hluav taws xob) thiab endogenous (ib txwm metabolic dab nyob rau hauv cov kab mob nyob) qhov chaw ntawm oxidative kev nyuaj siab tsim reactive oxygen hom (ROS). Endogenously, ROS yog generated raws li cov khoom ntawm biochemical tshuaj nyob rau hauv lub mitochondria (electron-transport system; ETS), plasma membrane, cytoplasm (xws li peroxisomes thiab lysozymes), thiab daim nyias nyias ntawm endoplasmic reticulum. Lub mitochondrial ETS, adenine dinucleotide phosphate (NADPH) oxidase, xanthine oxidase, myeloperoxidase, thiab endothelial nitric oxide synthase (eNOS) yog lub hauv paus tseem ceeb ntawm cellular ROS tsim. Cov tshuaj tiv thaiv tseem ceeb hauv kev tsim dawb radical yog Fenton thiab Fenton zoo li cov tshuaj tiv thaiv los tsim ROS uas Fe2 ntxiv thiab Cu ntxiv ua rau H2O2 tsim OH, raws li. Txhawm rau tiv thaiv thiab kho cov kab mob molecular raug mob los ntawm ROS, cov hlwb siv cov kab ke tiv thaiv uas muaj cov tshuaj tua kab mob enzymatic, suav nrog superoxide dismutase (SOD), catalase, peroxidase, thiab nonenzymatic antioxidants ua los ntawm glutathione system. Qhov chaw tseem ceeb ntawm O2•- tiam yog lub hauv paus mitochondrial membrane thaum ETS cov txheej txheem. Lub decomposition ntawm H2O2 rau hauv dej thiab oxygen yog ua los ntawm SOD, glutathione system, thiab catalase, nyob rau hauv qhov kev txiav txim. Tshaj ROS ua rau lipid peroxidation, nitro-oxidation, glycol-oxidation, thiab oxidative DNA puas, uas tuaj yeem ua ke ua rau cov protein hloov pauv, DNA puas, cellular senescence, thiab apoptosis. Tag nrho cov kev hloov no thaum kawg ua rau glomerulosclerosis thiab tubulointerstitial fibrosis.

Oxidative kev nyuaj siab yog koom nrog cov kab mob ntawm ntau lub raum kab mob, suav nrog mob raum raug mob (AKI), kab mob raum ntev (CKD), mob ntshav siab nephropathy, thiab ntshav qab zib nephropathy. Yog li ntawd, antioxidants yog cov cuab yeej zoo rau kev kho mob raum kab mob. Catalytic antioxidants yog cov molecule me me ntawm cov enzymes antioxidant zoo ib yam li SOD, CAT, thiab GPx, qee qhov tuaj yeem ua cov tshuaj tua kab mob rau lipid peroxides thiab ONOO-. Txij li cov tebchaw no yog catalytic thiab tsis yog cov dawb radical scavengers xwb, lawv pom muaj zog antioxidant zog dua li lwm cov khoom noj. Daim ntawv no tshuaj xyuas lub luag haujlwm ntawm antioxidant enzymes hauv cov kab mob raum, kev faib tawm ntawm catalytic antioxidants, thiab cov xwm txheej tam sim no ntawm lawv daim ntawv thov hauv cov kab mob raum.

Antioxidant Enzymes thiab kab mob raum

Cells muaj cov txheej txheem tiv thaiv antioxidant tseem ceeb los tiv thaiv lawv tus kheej los ntawm kev puas tsuaj ntawm cov dawb radicals. Antioxidants muaj peev xwm muaj endogenous los yog exogenous qhov chaw, nrog endogenous synthesis tsim enzymes thiab me me molecules los yog kev noj haus muab ib qho tseem ceeb exogenous tiv thaiv. Nyob ntawm lawv cov haujlwm, cov tshuaj tua kab mob antioxidant tuaj yeem raug cais ua enzymatic lossis tsis-enzymatic. Cov enzymatic antioxidants loj yog SOD, CAT, thiab GPx. Endogenous non-enzymatic antioxidants muaj xws li l-arginine, lipoic acid, coenzyme Q10, melatonin, albumin, thiab uric acid. Exogenous non-enzymatic antioxidants muaj xws li tshuaj xws li ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), phenolic antioxidants, lecithin roj, thiab acetylcysteine ​​​​. Ntau lub tshuab antioxidant kuj tseem muaj nyob rau hauv lub raum los tiv thaiv lub raum cov ntaub so ntswg thiab cov hlwb cuam tshuam los ntawm oxidative kev nyuaj siab.

Cistanche benefits

Cistanche ntxiv

1. Superoxide Dismutase thiab kab mob raum

Superoxide radical anion yog cov khoom muaj txiaj ntsig uas tsim los ntawm ib qho hluav taws xob txo qis ntawm cov pa oxygen molecular thaum ua pa.SOD yog qhov tseem ceeb antioxidant enzyme system thiab feem ntau cov kab mob nyob hauv lub xub ntiag ntawm oxygen nthuav tawm tsawg kawg yog ib qho SOD. Cov hlau ligand ntawm qhov chaw nquag tso cai rau kev faib tawm ntawm SOD: tooj liab-zinc SOD (Cu / Zn-SOD), manganese SOD (Mn-SOD), hlau SOD (Fe-SOD), thiab npib tsib xee SOD (NiSOD). SOD yog ib pawg ntawm metalloenzymes catalyze cov tshuaj tiv thaiv cleavage rau detoxify ROS, uas catalyzes cleavage ntawm ob O2- los tsim H2O2thiab molecular O2, uas yog decomposed rau hauv dej thiab oxygen los ntawm CAT.

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SOD kuj tau muab faib ua peb lub ntsiab isoforms raws li nws qhov chaw nyob hauv subcellular compartments: SOD1 (Cu/Zn-SOD), SOD2 (Mn-SOD), thiab SOD3 (extracellular SOD, EC-SOD), uas feem ntau pom nyob rau hauv lub raum. .SOD1 yog constitutively tam sim no nyob rau hauv lub cytoplasm thiab membrane gap ntawm mitochondria, thaum SOD2 yog tam sim no nyob rau hauv lub mitochondria ntawm eukaryotic hlwb. SOD3 yog Cu / Zn-SOD uas tau muab zais rau hauv qhov chaw extracellular. Ntawm peb SODs no, SOD1 muaj ntau nyob rau hauv cov ntaub so ntswg ntau, suav txog 60-80 feem pua ​​​​ntawm SOD kev ua hauv lub raum vasculature thiab kwv yees li 30 feem pua ​​​​ntawm SOD kev ua hauv lub raum vasculature.SOD2 kuj tau qhia hauv cov ntaub so ntswg feem ntau, xws li lub plab, lub ntsws, cov leeg pob txha, tus po, lub plawv, lub siab, lub raum, thiab lub hlwb.SOD3 tau qhia ntau heev hauv vasculature, raum, ntsws, thiab lub plawv. Txawm hais tias SOD1 suav txog qhov feem pua ​​​​ntawm SOD lub raum ua haujlwm siab tshaj plaws, cov kev hloov pauv pathological cuam tshuam nrog SOD2 deficiency thiab SOD1 deficiency yog qhov hnyav dua vim tias ROS thiab RNS yog tsim los ntawm mitochondria.

Tag nrho peb SOD isoforms ua lub luag haujlwm tseem ceeb hauv kev loj hlob thiab tshem tawm ntau yam kab mob raum. Ntau cov kev tshawb fawb sim muab pov thawj tias kev tshem tawm los yog overexpression ntawm sod los ntawm genetic manipulation los yog tshuaj yuav hloov oxidative kev nyuaj siab thiab kab mob hnyav nyob rau hauv AKI los yog CKD. SOD1 depletion ua rau muaj kev nce ntxiv hauv cov teeb meem nuclear  lub teeb saw txuas ntxiv (NF-κB) - kho lub raum teeb liab thiab oxidative DNA puas hauv cov hlwb B. Qhov tseeb, lub raum ua haujlwm tau txo qis tom qab lub raum ischemia-reperfusion (I / R) raug mob hauv SOD1 knockout nas, thiab kev kho tib neeg SOD1 rov ua tau txo qis ROS thiab txhim kho lub raum ua haujlwm los ntawm kev txo qis qog necrosis (TNF)- thiab interleukin (IL){ {7}} qib hauv lub raum I/R cov ntaub so ntswg raug mob. Hauv unilateral ureteral obstruction (UUO) nas, SOD1 tsis muaj peev xwm txhim kho ntsev-sensitive kub siab thiab tubulointerstitial fibrosis, whereas, nyob rau hauv unilateral ureteral obstruction nas b, SOD1 overexpression los yog mob ntev ntawm lub cev nqaij daim tawv abrogated cov kev tshawb pom no. sOD1 kuj hloov kho lub raum microvascular remodeling, me me hlab ntsha reactivity, thiab rhiab heev rau angiotensin II (Ang II). SOD1 knockout nas tau nthuav tawm cov ntshav siab thiab txo qis cov hlab ntsha me me thaum lub sij hawm Ang II infusion, whereas cov kev hloov no tau attenuated hauv SOD1 transgenic nas. Hauv kev mob ntshav qab zib nephropathy, qib siab glycosylation kawg cov khoom (AGEs) txhim kho oxidative kev nyuaj siab los ntawm NOX tiam ntawm ROS hauv mitochondria, thiab kev sib cuam tshuam ntawm AGEs thiab receptors rau AGEs (RAGE) txhim kho qhov pib ntawm cov teeb liab cuam tshuam. Antioxidant enzymes, xws li SOD thiab CAT, inhibit hnub nyoog-mediated ROS ntau lawm. Piv rau kev tswj cov nas mob ntshav qab zib, SOD1 transgenic db / db nas thiab STZ streptozotocin-kho SOD1 transgenic nas nthuav tawm txo cov proteinuria, hloov pauv kev loj hlob (TGF)- 1 thiab collagen IV kab lus, nrog rau thylakoid matrix expansion thiab txo cov cim ntawm oxidative kev nyuaj siab.

SOD2 tsis ua haujlwm tau raug tshaj tawm tias ua rau lub raum tsis ua haujlwm, tubulointerstitial fibrosis, o, thiab lub raum apoptosis. Parajuli et al. pom tias lub raum tshwj xeeb SOD2- cov nas uas tsis muaj zog muaj lub raum sib zog thiab me dua li cov nas qus uas muaj kev txhim kho oxidative kev nyuaj siab thiab kev raug mob ntawm tubular, nrog rau qhov distal tubular dilatation, protein cast formation, thiab distal tubular epithelial cell o. Hauv lub raum I / R raug mob, SOD2 qhia tau txo qis hauv lub raum lub raum thiab lub raum kev ua haujlwm tsis zoo nyob rau hauv SOD2 knockout nas piv rau cov nas. Nyob rau hauv tus qauv nas ntawm radiocontrast-induced AKI, recombinant SOD2 pretreatment ho nce SOD kev ua si thiab ameliorated txo lub raum ua haujlwm thiab tubular necrosis. Tsis tas li ntawd, kev noj zaub mov muaj ntsev ntau hauv cov kua qaub2- cov nas tsis muaj peev xwm ua rau muaj kev nce siab hauv cov hlab ntsha thiab cov zis albumin tawm los ntawm kev tswj hwm ntawm NOX thiab ua kom NF-κB. Lwm txoj kev tshawb fawb kuj tau qhia tias qhov tsis txaus SOD2 ua rau muaj kev cuam tshuam ntau ntxiv thiab ua rau cov kab mob glomerulosclerosis, tubulointerstitial raug mob, thiab ntsev-sensitive kub siab, tshwj xeeb tshaj yog cov nas muaj hnub nyoog. Cov txheej txheem tsim los ntawm cov kws sau ntawv no rau kev ua haujlwm tsis zoo ntawm microvascular yog qhov tsis txaus SOD2 nce O2-- theem thiab impairs ntws thiab agonist-induced vasodilation hauv cov hlab ntsha mesenteric cais.

Ntau dhau mitochondrial O2- kev tsim khoom thiab kev cuam tshuam mitochondrial tsis ua haujlwm yog txuam nrog cov kab mob ntawm cov ntshav qab zib nephropathy. Ntau qhov kev sim tau tshaj tawm txo qis kev ua haujlwm SOD2 hauv cov tsiaj qauv ntawm hom 1 thiab hom 2 mob ntshav qab zib nephropathy. Hauv qhov sib piv, lwm cov kev tshawb fawb qhia tsis muaj qhov sib txawv tseem ceeb hauv SOD2 qhia ntawm cov kab mob ntshav qab zib thiab tswj cov nas. Dugan et al. pom muaj zog rau lub raum ROS hauv SOD2-cov nas mob ntshav qab zib tsis txaus, tab sis lawv tsis pom muaj pov thawj ntawm kev nce proteinuria lossis thylakoid stromal expansion. Yog li, lub luag haujlwm ntawm SOD2 hauv ntshav qab zib nephropathy yog qhov tsis sib haum xeeb thiab xav tau kev tshawb fawb ntxiv los txiav txim siab txog lub luag haujlwm ntawm SOD2 hauv cov ntshav qab zib nephropathy.

Raws li nrog SOD1 thiab SOD2, ntau qhov kev tshawb fawb tau siv SOD3 knockout tsiaj qauv los ua kom pom lub luag haujlwm ntawm SOD3 hauv kev tiv thaiv lossis ua kom lub raum raug mob hauv kev teb rau oxidative kev nyuaj siab. Tom qab lub raum cov hlab ntsha clipping hauv SOD3 knockout nas, Ang II kev kho mob ua rau kom ntshav siab ntxiv thiab ua rau endothelial tsis ua haujlwm, thiab kev kho SOD3 recombinant xaiv txo cov ntshav siab SOD3 knockout nas [44 ntshav siab. Lwm txoj kev tshawb fawb tau tshaj tawm tias SOD3 feem ntau nyob hauv cheeb tsam rau cov tubule ze ze thiab sib koom nrog erythropoietin (EPO). Piv nrog rau kev tswj cov tsiaj, cov nas hypoxia-exposed SOD3 knockout nas pom qhov nce me me ntawm EPO qib thiab tsawg zuj zus ntawm nuclear translocation hypoxia-inducible factor (HIF)-1 . Raws li qhov kev tshawb pom no, SOD3 tshem tawm retarded raum cov ntshav ntws rov qab los tom qab lub raum ischemia thiab ua rau cov tubular necrosis thiab tubular cast formation tom qab reperfusion.SOD3 knockout nas kuj pom muaj proteinuria, lub raum fibrosis, thiab podocyte raug mob tom qab kho adriamycin, ib qho kev sim qauv ntawm focal. segmental glomerulosclerosis (FSGS), ib qho kev tshawb pom txuam nrog NOX2 thiab -catenin signaling pathway tau txuam nrog upregulation ntawm NOX2 thiab -catenin signaling pathways. Yog li, SOD3 plays lub luag haujlwm tseem ceeb hauv kev tiv thaiv lub raum hauv ntau yam kab mob raum.

Cistanche benefits

Herba Cistanche

Txhawm rau ntsuas lub luag haujlwm ntawm SOD isoforms hauv ntshav qab zib nephropathy, Fijuta li al. Kev soj ntsuam SOD kev ua thiab SOD isoform qhia hauv lub raum ntawm tus qauv mob ntshav qab zib nas thiab pom tias SOD1 thiab SOD3 tau txo qis hauv cov ntshav qab zib raum, tab sis SOD2 tsis yog. Tib pab pawg tau tshaj tawm siv SOD1- thiab sod3-knockout nas ntshav qab zib kom paub meej lub luag haujlwm tshwj xeeb ntawm SOD isoforms hauv ntshav qab zib nephropathy. Lawv xaus lus tias hauv C57BL/6-Akita mob ntshav qab zib nas, SOD1 tsis txaus tab sis tsis muaj SOD3 tsis txaus ua rau lub raum O2 - thiab ua rau lub raum raug mob loj - thiab SOD1 ua lub luag haujlwm tseem ceeb tshaj SOD3 hauv cov kab mob ntshav qab zib. nephropathy. Txawm li cas los xij, kev tshawb fawb tsis ntev los no tau tshaj tawm lub luag haujlwm ywj pheej rau SOD3 hauv kev tiv thaiv kab mob ntshav qab zib nephropathy. Peb txoj kev tshawb fawb tau pom tias SOD3 qhia nyob rau hauv glomerular thiab tubular cheeb tsam ntawm db / db nas tau nce ntxiv tom qab recombinant human SOD3 supplementation. Hauv cov qauv tsiaj ntawm hom 1 thiab hom 2 mob ntshav qab zib nephropathy, recombinant human SOD3 supplementation txhim kho qhov kev qhia ntawm SOD3 los ntawm inhibiting phosphorylation ntawm ROS thiab extracellular signal-regulated kinase (ERK) 1/2 los yog intrarenal 5 ' - amp activated protein kinase-peroxisome proliferator -activated receptor coactivator (PGC)-1 -nuclear factor erythroid 2-related factor (Nrf)2 activation of signaling pathways to improve diabetes nephropathy. Yog li, kev sim ntxiv yog xav tau los piav qhia lub luag haujlwm ywj pheej ntawm SOD3 hauv kev tiv thaiv ntshav qab zib nephropathy.

2. Kab mob Catalase thiab raum

CAT yog 240 kDa heme-muaj homotetrameric protein nyob hauv cov peroxisome thiab muaj ntau nyob rau hauv daim siab, ntsws, thiab lub raum. Nyob rau hauv lub raum, CAT feem ntau yog faib nyob rau hauv lub cytoplasm ntawm lub proximal tubules ntawm lub paramedian cortex thiab yog tsawg qhia nyob rau hauv lub proximal tubules ntawm lub superficial cortex. Ntawm qhov tod tes, CAT tsis muaj nyob rau hauv lub glomeruli, distal tubules, collaterals ntawm Hench, los yog sau ducts.CAT deficiency ua rau mitochondrial ROS overexpression thiab functional mitochondrial puas tsuaj.CAT txo H2O2 tsim los ntawm SOD rau oxygen thiab dej. Txawm hais tias CAT muaj txiaj ntsig zoo hauv kev txo H2O2, nws lub luag haujlwm hauv kev tswj hwm H2O2 yuav tsis yog lub hauv paus, vim nws feem ntau nyob hauv peroxisome.

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CAT deficiency tau raug tshaj tawm tias ua rau kom muaj tubulointerstitial fibrosis thiab lipid peroxidation khoom ntawm tubulointerstitial lesions hauv UUO nas. Kobayashi et al. pom tau hais tias CAT txo lub raum ua haujlwm thiab ua kom lub raum mob hnyav dua los ntawm kev hloov pauv ntawm epithelial-rau-mesenchymal hloov ntawm lub raum nyob rau hauv 5/6 nephrectomized nas. Tsis tas li ntawd, piv nrog cov nas qus, adriamycin-kho nas nrog cov ntshav poob ua rau cov proteinuria hnyav, ua kom cov glomerulosclerosis thiab tubulointerstitial fibrosis, thiab nce lipid peroxidation tsub zuj zuj.

Hauv kev mob ntshav qab zib nephropathy, proximal tubule-specific CAT overexpression hauv STZ-kho mob ntshav qab zib nas thiab db/db nas inhibited lub raum ROS tiam thiab tubular interstitial fibrosis thiab attenuated angiotensinogen, p53, thiab pro-apoptotic Bcl-2-BAX protein (BAX) ) gene expression. Raws li cov kev tshawb fawb no, CAT overexpression nyob rau hauv Akita nas txo qis systolic ntshav siab los ntawm kev tswj lub intrarenal renin-angiotensin system (RAS), txhim kho angiotensin-hloov enzyme (ACE) 2, inhibiting ACE thiab angiotensinogen qhia, los yog los ntawm activating nuclear factor erythroid. 2-related factor 2 (Nrf2)-heme oxygenase (HO){12}} signaling pathway. Godin et al. siv proximal tubule-specific CAT thiab/los yog angiotensinogen transgenic nas kom paub meej tias lub koom haum ntawm CAT thiab intrarenal RAS kev ua hauv kev txhim kho ntshav siab thiab mob raum. Lwm tus kws tshawb fawb kuj tau tshaj tawm tias CAT deficiency ua rau mob ntshav qab zib nephropathy los ntawm kev ua rau peroxisome / mitochondrial biogenesis thiab fatty acid oxidation. Yog li, endogenous CAT muaj lub luag haujlwm tseem ceeb tiv thaiv kab mob ntshav qab zib nephropathy los ntawm kev tswj cov kab mob hauv lub cev RAS thiab peroxisome metabolism thiab txo cov kev ntxhov siab oxidative.

3. Glutathione Peroxidase thiab kab mob raum

Lwm H2O2 scavenger, GPx, converts peroxides thiab OH- rau cov khoom tsis muaj tshuaj lom los ntawm oxidizing txo glutathione (GSH) rau glutathione disulfide (GSSG), uas tom qab ntawd txo glutathione los ntawm glutathione reductase ntawm NADPH.GPx synergizes nrog CAT kom tawg H.2O2rau H2O thiab oxidizes glutathione, uas yog txo los ntawm glutathione reductase. GPx xav kom GSH ua hydrogen pub rau catabolize H2O2rau dej thiab oxygen thiab yuav tsum tau selenium (Se) ua ib cofactor los koom rau hauv cov tshuaj tiv thaiv nrog peroxides.

GPx yog tetrameric protein nyob rau hauv txhua lub monomer muaj Se atom ntawm qhov chaw catalytic. Txhua monomer muaj selenocysteine ​​​​, qhov twg sulfur hauv cysteine ​​​​tau hloov los ntawm selenium (R-SeH). Thoob plaws hauv lub voj voog catalytic, selenol (protein Se-) reacts nrog hydrogen peroxide (H2O2los yog lipid hydrogen peroxide, LOOH) los tsim selenite (protein- SeOH). Selenious acid regenerates selenol ntawm ob GSHs, uas nws thiaj li oxidized rau GSSG thiab LOOH. LOOH raug txo mus rau qhov sib thooj lipid cawv (LOH).

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Txog hnub tim, yim GPx sib txawv tau raug txheeb xyuas hauv cov tsiaj txhu; Txawm li cas los xij, tsuas yog tsib isoforms muaj selenocysteine ​​thiab yuav tsum tau siv glutathione los ua cov cofactor kom txo qis H2O2 thiab LOOH (GPx 1-4 thiab 6). Nyob rau hauv lub raum, loj npaum li cas ntawm GPx muaj nyob rau hauv lub proximal thiab distal tubules thiab cov nqaij mos hlwb ntawm lub raum cov hlab ntsha. ntawm GPx isoforms, GPx1 thiab GPx4 feem ntau yog qhia hauv podocytes thiab thylakoid hlwb; GPx3 yog tsim nyob rau hauv qab daus daim nyias nyias ntawm lub proximal thiab distal tubules ntawm lub raum cortex; GPx2 thiab GPx5 tsis kuaj pom hauv lub raum. GPx1, qhov ntxov tshaj plaws txheeb xyuas cov noob, yog qhov kev qhia siab, thiab nws lub luag haujlwm hauv kev txo qis oxidative kev nyuaj siab tau pom dav dav. GPx1 feem ntau pom muaj nyob rau hauv lub raum ib txwm thiab suav txog 96 feem pua ​​​​ntawm lub raum GPx kev ua haujlwm. Esposito et al. pom tau hais tias GPx1 muaj ntau qhia nyob rau hauv lub mitochondria ntawm lub raum cortex thiab hais tias GPx1 deficiency txo lub cev hnyav thiab exacerbates ib endogenous, hnub nyoog-dependent poob nyob rau hauv tag nrho cov cellular muaj nuj nqi. Yog li, txoj cai ntawm lub raum GPx1 tau xav tias ua lub luag haujlwm tseem ceeb hauv kev tiv thaiv lub raum los ntawm kev ntxhov siab oxidative.

Cistanche benefits

Cistanche extract

Ntau qhov kev tshawb fawb yav dhau los tau soj ntsuam cov teebmeem nephroprotective ntawm GPx1 hauv lub raum kab mob.GPx1 gene inhibition exacerbates cocaine-induced AKI los ntawm inhibiting phosphoinositide kinase (PI3K)-Akt signaling pathway to activate the angiotensin II type 1 receptor (AT1x). overexpression ameliorates oxidative kev nyuaj siab thiab mitochondrial ROS nyob rau hauv cov nas laus los ntawm attenuating glomerulosclerosis [74]. Hauv ntshav qab zib nephropathy, Chiu et al. qhia tias cov ntshav plasma thiab urinary GPx qib tau qis dua hauv cov neeg mob ntshav qab zib glomerulosclerosis ntau dua li cov neeg mob uas tsis yog glomerulosclerosis thiab cov glomerular GPx qhia tau qis dua hauv cov nas mob ntshav qab zib ntau dua li cov nas tswj ib txwm. Txawm li cas los xij, GPx1-cov nas mob ntshav qab zib tsis txaus tau nthuav tawm cov qib zoo sib xws ntawm kev puas tsuaj oxidative, glomerular puas, thiab lub raum fibrosis raws li kev tswj cov nas mob ntshav qab zib, thiab GPx1 deficiency tsis yog endogenously compensated los ntawm kev nce hauv CAT lossis lwm yam GPx isoforms thaum lub sijhawm ntxov ntawm kev mob ntshav qab zib. nephropathy. txhim kho GPx kev ua si thiab GPx carboxylation tsis tau nrog los ntawm kev nthuav qhia GPx hauv ob lub raum ntawm cov nas me me uas muaj ntshav qab zib. Qhov kev qhia thiab kev ua ntawm GPx1 thiab GPx4 tsis txawv ntawm ob lub raum ntawm cov laus mob ntshav qab zib thiab cov nas uas tsis yog ntshav qab zib. Hauv kev sib piv, Chew et al. pom tau hais tias GPx1 tsis muaj peev xwm nce proteinuria hauv cov ntshav qab zib ApoE / GPx1 ob lub khob nas, uas tau cuam tshuam nrog nce glomerular thylakoid matrix expansion thiab upregulation ntawm mediators ntawm o thiab fibrosis. Yog li, cov nyhuv nephroprotective ntawm GPx1 hauv ntshav qab zib nephropathy tseem tsis paub meej.

GPx3 yog ib qho tshuaj antioxidant selenoprotein, tseem hu ua plasma GPx. GPx3 yog synthesized feem ntau nyob rau hauv sab nrauv lumen ntawm lub raum puag thiab khi rau hauv qab daus daim nyias nyias ntawm lub raum cortical epithelial hlwb. GPx3 tseem khi rau hauv qab daus daim nyias nyias ntawm cov kab mob extrarenal epithelial nyob rau hauv txoj hnyuv, lub ntsws, thiab epididymis ntawm cov hlab ntsha. Cov kev tshawb pom no qhia tias GPx3 tsis muaj peev xwm tshwm sim los ntawm lub raum raug mob tuaj yeem cuam tshuam rau hauv nruab nrog cev. Hauv kev phais mob CKD qauv, GPx3 tsis muaj peev xwm txo qis kev muaj sia nyob thiab txhawb nqa sab laug ventricular tsis ua haujlwm, raws li ROS tsub zuj zuj zuj zus ua rau muaj teeb meem inflammatory thiab platelet activation. Yog li, GPx3 tuaj yeem ua lub luag haujlwm tseem ceeb hauv kev sib tham ntawm lub raum thiab lwm yam kabmob.

Tsis ntev los no, ferroptosis, ib tug hlau-dependent programmed cell tuag tus cwj pwm los ntawm tsub zuj zuj ntawm lipid hydroperoxides mus rau theem tuag, tau raug tshaj tawm hais tias muaj kev koom tes nyob rau hauv lub pathophysiology ntawm ob peb lub raum kab mob.GPx4 yog lub ntsiab enzyme uas thaiv ferroptosis, thiab GPx4 inhibitors induce ferroptosis. cell tuag los ntawm kev khi thiab inactivating GPx4.GPx4 deficiency kuj exacerbates AKI los ntawm kev ua kom intracellular LOOH thiab txhawb cov hlau ua cell tuag exacerbates AKI; lipo statin-1 tiv thaiv GPx4 depletion-induced raum raug mob. Ib txoj kev tshawb fawb tsis ntev los no tau pom qhov nce qib ntawm acyl-coenzyme A synthase ntev-chain hauv tsev neeg 4 (ACSL4) thiab txo qis ntawm GPx4 hauv cov nas mob ntshav qab zib, thiab cov kev tshawb pom no qhia tias hlau sagging yog koom nrog hauv pathogenesis ntawm ntshav qab zib nephropathy [85] . Txog niaj hnub no, tsis tau muaj kev koom tes ntawm GPx2 thiab GPx5 thiab kab mob raum.

Cov ntaub ntawv

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Yim Ah Hong1thiab Cheol Whee Park1,2,

1 Department of Internal Medicine, College of Medicine, Catholic University of Kauslim, Seoul 06591, Kauslim; amorfati@catholic.ac.kr

2 Lub Tsev Kawm Ntawv rau Kev Laus thiab Metabolic Diseases, Tsev Kawm Qib Siab Tshuaj, Lub Tsev Kawm Qib Siab Catholic ntawm Kaus Lim Kauslim, Seoul 06591, Kauslim


Koj Tseem Yuav Zoo Li