Cov teebmeem ntawm Tag Nrho Glycosides Ntawm Cistanche Ntawm O Xidative Stress Injury Thiab Apoptosis hauv nas Nrog Cerebral Ischemia - Reperfusion Ⅱ

2 kev tshwm sim

2. 1 Kev sib piv ntawm cov qhab nia neurological deficit

Piv nrog rau pawg Sham, nas hauv Mod⁃el pab pawg muaj ntau duaCov tsos mob ntawm neurological deficit loj heevthiabnce neurological deficit qhab nia(P ＜0. 05); piv nrog rau pawg qauv, cov nas hauv pawg GCs tau siab dua Cov qhab nia ntawm cov paj hlwb poob qis (P<0. 05), see Figure 1.

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2. 2 TTC staining tshwm sim ntawm lub paj hlwb

Tsis muaj qhov pom tseeb ntawm qhov txhab mob hauv lub hlwb ntawm cov nas hauv pawg Sham. Nyob rau hauv kev sib piv, qhov feem pua ​​​​ntawm cov paj hlwb infarction cheeb tsam hauv cov nas nyob rau hauv pawg Model yog loj dua (P < 0.01); Qhov feem pua ​​​​ntawm cov paj hlwb infarction nyob rau hauv cov nas nyob rau hauv cov pab pawg neeg kho GCs yog qis dua li hauv pawg Model. (P<0. 05), see Figure 2.

2. 3 Kev sib piv ntawm oxidative stress indicators

Piv nrog rau pawg Sham, MDA cov ntsiab lus nyob rau hauv cov ntshav ntawm cov nas nyob rau hauv Model pawg tau nce, thiab cov dej num ntawm cov tshuaj antioxidant SOD thiab GSH-Px poob qis (P < 0.05); thaum cov nas nyob rau hauv pawg GCs piv nrog cov M pawg nas hauv pawg odel, Cov ntsiab lus MDA poob qis, thiab cov haujlwm ntawm SOD thiab GSH-Px nce (P < 0. 05), saib Table 1.

3 Kev sib tham

Nws paub tias ntau yam thiab ntau qhov txuas tau koom nrog hauv cov paj hlwb tom qab necrosis tshwm sim los ntawm CIRI. Inhibiting qhov tshwm sim thiab kev loj hlob ntawm cov txheej txheem pathological nyob rau hauv ib lub sij hawm zoo ntawm lub sij hawm yog heev tseem ceeb heev rau cov prognosis ntawm tus kab mob. Wang et al. [4] luam tawm Daim duab 3. Kev sib piv ntawm Bax, Bcl-2, Caspase-3, HO-1, thiab Nrf2 protein qhia nyob rau hauv lub hlwb cov ntaub so ntswg ntawm nas nyob rau hauv txhua pab pawg neeg. Nco tseg: Piv nrog rau pawg neeg ua haujlwm sham, ∗ Ｐ＜0. 0５,∗∗Ｐ＜0. {{10}}1; piv nrog rau pawg qauv, #P < 0. 0５,##P＜0. 01 Kev txhim kho ntawm cov paj hlwb tsis txaus thiab cerebral infarction cheeb tsam ntawm CIRI nas tom qab kev kho GCs tau lees paub tias nws cuam tshuam rau lub hlwb puas thiab tom qab kev mob tshwm sim.

CovCov txiaj ntsig zoo ntawm kev rov ua haujlwm ntawm lub cev muaj zog; Cov txiaj ntsig ntawm qhov kev sim no kuj tau ua pov thawj tias cov qhab nia ntawm cov paj hlwb tsis txaus ntawm cov nas tom qab CIRI kev kho mob nrog GCs raug txo, thiab feem pua ​​​​ntawm cov paj hlwb infarction cheeb tsam raug txo, qhia tias GCs muaj kev tiv thaiv lub hlwb puas tom qab CIRI.

Raws li kev tswj hwm tseem ceeb koom nrog hauv cov tshuaj tiv thaiv redox hauv cov hlwb, Nrf 2 plays lub luag haujlwm tseem ceeb hauv kev tshwm sim ntawm ntau yam kab mob, xws li cov kab mob neurodegenerative, qog, laus, thiab lwm yam. 9].

Nws exerts nws cov nyhuv antioxidant los ntawm kev sib txuas nroganti-oxidant teb cov ntsiab lus(TSIS) txhawbdownstream SOD, Kev nthuav qhia ntawm CAT thiab GSH-Px [10]. HO-1 ua haujlwm raws li kev tswj hwm cov protein ntawm Nrf 2/ARE txoj hauv kev, thiab nws qhov kev ua kom muaj peev xwm pib ua kom muaj zog tiv thaiv oxidative, tiv thaiv kev mob, thiab

Kev tiv thaiv mechanism tiv thaiv cell puas [11]. HO-1 tuaj yeem txhawb nqa oxidative degradation ntawm heme thiab neutralize ntau cov pa oxygen reactive. Nws upregulation yog ib qho tseem ceeb mechanism rau cov hlwb hloov mus rau oxidative kev nyuaj siab. HO-1 tuaj yeem tiv taus qhov kev puas tsuaj los ntawm oxidative kev nyuaj siab rau lub cev, yog litxo cell apoptosis [12].

Tom qab CIRI tshwm sim, kev tsim tawm ntau dhau ntawm cov pa dawb radicals yuav ua rau muaj qhov tsis txaus ntseeg hauv lawv cov khoom tsim thiab degradation, thiab cov tsub zuj zuj ntawm cov pa oxygen reactive yuav ua rau cov hlwb raug tawm tsam los ntawm ntau hom reactive oxygen. SOD thiab GSH-Px yog ib qho tseem ceeb antioxidant yam, thiab lawv qhov tsis tuaj yeem txhawb nqa lipid peroxidation, thiab kev tsim cov tshuaj cytotoxic MDA yuav nce ntxiv, ua rau muaj kev ua haujlwm ntawm tes thiab ua rau lub hlwb puas tsuaj [13].

Wang et al. [14] pom tias los ntawm kev nce cov dej num ntawm SOD, CAT thiab GSH-Px thiab txo cov ntsiab lus ntawm MDA thiab protein hydroxyl pawg, cov tshuaj antioxidant muaj peev xwm ntawm cov ntshav, daim siab thiab lub hlwb tuaj yeem txhim kho. Ye Hongxia et al. [15] pom nyob rau hauv kev tshawb fawb txog cov nyhuv nootropic ntawm GCs ntawm cov nas uas nws txo qis kev puas tsuaj rau lub hlwb cov qauv thiab ua haujlwm los ntawm kev ua kom muaj zog antioxidant enzyme thiab txo qis oxidative kev ntxhov siab. Cov kev tshawb fawb yav dhau los los ntawm Wang et al. [4] lees paub tias GCs kev kho mob txhawb nqa neuronal remodeling thiab angiogenesis. Cov txheej txheem yuav cuam tshuam rau kev ua kom Nrf 2 txoj hauv kev thiab txo qis oxidative kev ntxhov siab ntawm cov ntaub so ntswg hlwb. Cov txiaj ntsig ntawm qhov kev sim no tau pom tias GCs tau tswj hwm qhov kev qhia ntawm Nrf 2 thiab nws lub hom phiaj nqes hav protein HO-1, nce kev ua haujlwm ntawm antioxidant enzymes SOD thiab GSH-Px hauv cov ntaub so ntswg hauv hlwb, ua kom cov pa oxygen dawb radicals. , thiab kuj txo cytotoxicity. Lub tsub zuj zuj ntawm cov tshuaj MDA, yog li txo oxidative kev nyuaj siab-induced hlwb puas.

Wu Jiangli et al. [16] tau qhia tias Nrf 2 tseem tuaj yeem tswj hwm txoj hauv kev mitochondria-mediated endogenous apoptosis, tswj kev qhia ntawm cov proteins Bax thiab Bcl-2 thiab inhibit apoptosis. Cov kev tshawb fawb tau pom tias GCs tuaj yeem txhim kho kev qhia ntawm Bcl -2 hauv cov ntaub so ntswg myocardial, txo qis- tswj kev qhia ntawm Bax thiab Caspase-3, txo cov apoptosis los ntawm ischemia-reperfusion, thiab yog li txo cov myocardial. kev puas tsuaj [17].

Hauv kev tshawb fawb txog kev cuam tshuam ntawm GCs ntawm cov qog loj hlob thiab cov kab mob metastasis, nws tau pom tias lawv siv cov nyhuv pro-apoptotic los ntawm kev tswj cov kev qhia ntawm Bax thiab Bcl -2 proteins. Tom qab kev loj hlob ntawm cov hlwb endothelial yog inhibited, tsim cov hlab ntsha kuj txo qis [18] . Cov txiaj ntsig ntawm qhov kev sim no tau pom tias kev cuam tshuam GCs tau nce qhov kev qhia ntawm cov tshuaj tiv thaiv apoptotic Bcl -2 thiab txo qhov kev qhia ntawm pro-apoptotic proteins Bax thiab Caspase -3 hauv lub hlwb, ua pov thawj tag nrho. nws zoo txhawb kev ciaj sia ntawm paj hlwb. nyhuv.

Hauv cov ntsiab lus, GCs tuaj yeem txhim kho lub peev xwm ntawm cov paj hlwb hauv thaj chaw ischemic penumbra los tiv thaiv oxidative kev nyuaj siab puas tsuaj thiab txo cov paj hlwb apoptosis los ntawm CIRI los ntawm kev ua kom Nrf 2/HO-1 txoj hauv kev, qhia tias GCs yuav yog ib hom. Cov tshuaj muaj peev xwm rau kev kho mob ntawm lub hlwb raug mob tom qab cerebral ischemia-reperfusion.

Cov ntaub ntawv

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