本文選題：Herkinorin + 后處理　； 參考：《首都醫(yī)科大學(xué)學(xué)報(bào)》2017年03期

【摘要】：目的探討非阿片類阿片受體激動(dòng)劑Herkinorin后處理的腦保護(hù)作用以及典型蛋白激酶Cγ(conventional protein kinase Cγ,c PKCγ)的作用。方法成年雄性C57BL/6小鼠按數(shù)字表法隨機(jī)分為對(duì)照組(Naive),假手術(shù)組(Sham),模型組(ischemia/reperfusion,I/R),溶劑組(I/R+D,再灌注前腹腔注射同等劑量的DMSO),Herkinorin組(I/R+H,再灌注前腹腔注射10 mg/kg Herkinorin)。應(yīng)用小鼠腦中動(dòng)脈阻塞(middle cerebral artery occlusion,MCAO)誘導(dǎo)缺血性腦卒中模型,通過(guò)神經(jīng)行為和運(yùn)動(dòng)功能檢測(cè)評(píng)估腦損傷程度,借助2,3,5-氯化三苯基四氮唑(2,3,5-triph-enyltetrazolium chloride,TTC)染色觀察腦梗死體積,蛋白印跡檢測(cè)c PKCγ膜轉(zhuǎn)位(激活)水平。結(jié)果與I/R組比較,I/R+H組缺血再灌注后24 h和7 d的神經(jīng)行為評(píng)分明顯降低,爬桿實(shí)驗(yàn)、圓柱體實(shí)驗(yàn)和步錯(cuò)實(shí)驗(yàn)測(cè)評(píng)明顯改善(P0.05,n=6)。TTC染色顯示I/R組梗死體積24 h為31.44%±5.44%,7 d為23.44%±7.95%,I/R+H組(24 h:17.19%±3.23%,7 d:13.26%±2.71%)腦梗死體積明顯減少(P0.05,n=6)。Western blotting結(jié)果顯示,I/R組缺血核心區(qū)(Ic)和半影區(qū)(P)中c PKCγ膜轉(zhuǎn)位水平都明顯下降,而Herkinorin可明顯減輕MCAO小鼠半影區(qū)內(nèi)c PKCγ膜轉(zhuǎn)位水平的降低(P0.05,n=6)。結(jié)論 10 mg/kg Herkinorin腹腔注射能減輕MCAO小鼠皮質(zhì)的缺血再灌注損傷,c PKCγ膜轉(zhuǎn)位水平的變化可能參與Herkinorin后處理腦保護(hù)的分子機(jī)制。
[Abstract]:Objective to investigate the protective effect of non-opioid receptor agonist Herkinorin on brain and the role of typical protein kinase C 緯 conventional protein kinase C 緯 PKC 緯. Methods Adult male C57BL/6 mice were randomly divided into control group, sham group, model group, solvent group, I / R / R group. The same dose of Herkinorin group was injected intraperitoneally before reperfusion, and 10 mg/kg Herkinorin group was intraperitoneally injected with 10 mg/kg Herkinorin before reperfusion. Middle cerebral artery occlusion (MCAO) was used to induce ischemic stroke model in mice. The degree of cerebral injury was evaluated by neurobehavioral and motor function tests. The infarct volume was observed by the staining of 2ttriph-enyltetrazolium chloridetrichlorotetrazolium chloridetrichloroate (TTC). The level of c PKC 緯 membrane translocation (activation) was detected by Western blot. Results compared with the I / R group, the neurological behavior scores of I / R H group decreased significantly 24 and 7 days after ischemia and reperfusion. Cylinder experiment and treadmill test showed that the infarct volume in I / R group was 31.44% 鹵5.44% in 24 h, 23.44% 鹵7.95% 鹵7.95% in 7 days.) the infarct volume in I / R group was significantly reduced by P0.05 ~ (5) ~ (6)% 鹵2.71%). Western blotting showed that c PKC 緯 was found in the ischemic core area and penumbra in the I / R group. (P = 17.19% 鹵3.23% 鹵13.26% 鹵2.71% at 24 h). Western blotting showed that the infarct volume of I / R group was significantly lower than that of P0. 05% ~ (6)%. Western blotting showed that c PKC 緯 was found in the ischemic core area and penumbra area in the I / R group. The membrane translocation level decreased obviously, Herkinorin could significantly reduce the level of c PKC 緯 membrane translocation in penumbra of MCAO mice. Conclusion Intraperitoneal injection of 10 mg/kg Herkinorin can attenuate the changes of c PKC 緯 membrane translocation in the cortex of MCAO mice after ischemia reperfusion injury, which may be involved in the molecular mechanism of brain protection after Herkinorin treatment.
【作者單位】： 首都醫(yī)科大學(xué)附屬北京同仁醫(yī)院麻醉科;首都醫(yī)科大學(xué)基礎(chǔ)醫(yī)學(xué)院神經(jīng)生物學(xué)系;
【基金】：國(guó)家自然科學(xué)基金(81301065) 北京市優(yōu)秀人才培養(yǎng)資助計(jì)劃(D003034000031) 首都醫(yī)科大學(xué)附屬北京同仁醫(yī)院科研骨干培育基金(2014-YJJ-GGL-044)~~
【分類號(hào)】：R743.3

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