目的 以細(xì)胞凋亡和應(yīng)激平衡損傷為切入點(diǎn)探討舒腦欣滴丸（SNX）對(duì)腦缺血損傷大鼠急性后期的保護(hù)作用。方法 采用大鼠大腦中動(dòng)脈電凝法制備腦卒中模型，造模成功大鼠隨機(jī)分為5組，模型組、腦心通膠囊0.5 g/kg組和SNX 13、26、52 mg/kg組以及，每組10只，另設(shè)假手術(shù)組10只。腦缺血后48 h開始ig給藥，每天1次，連續(xù)2 d。試劑盒法檢測血清血管活性物質(zhì)內(nèi)皮素（ET）、一氧化氮（NO）活性，測定血清氧化應(yīng)激因子超氧化物歧化酶（SOD）/丙二醛（MDA）水平；TUNEL染色測定細(xì)胞凋亡率，免疫組化法測定細(xì)胞凋亡相關(guān)蛋白Bcl-2/Bax比值、以及Caspase-3蛋白表達(dá)變化。結(jié)果 與模型組比較，SNX能一定程度減少細(xì)胞凋亡率，且可不同程度降低凋亡蛋白平衡Bax/Bcl-2比值；顯著降低Caspase-3促凋亡蛋白因子的表達(dá)（P<0.01、0.001）；可調(diào)節(jié)氧化/抗氧化平衡，顯著提高SOD/MDA值（P<0.05），并顯著增加血管活性物質(zhì)NO/ET比值（P<0.01）。結(jié)論 SNX對(duì)大鼠腦缺血急性晚期損傷引起的細(xì)胞凋亡及應(yīng)激平衡失衡具有一定的改善作用。

Objective With apoptosis and stress balance injury as the entry point, to study the therapeutic effect of Shunaoxin Dropping Pill (SNX)on acute late stage of cerebral ischemic injury in rats. Methods The middle cerebral artery injury model was established by the electrocoagulation to prepare acute late-stage model of stroke in rats. Rats were equally divided into five groups (i.e model group, three SNX groups with 13, 26, and 52 mg/kg, positive control groups with NaoXinTong Capsule with 10 rats in each group. In addition, 10 rats without electrocoagulation were arranged as Sham group. The drug was administered on the 2nd day after cerebral ischemia, Each group was treated with corresponding drugs once daily for 2d. Serum NO and ET were measured by chemical method and enzyme linked immunosorbent assays. The oxidative stress cytokines involving serum SOD, MDA were measured by chemical methods. Cell apoptosis rates was determined by TUNEL staining, and the expression of apoptosis-related protein Bcl-2/Bax and the expression of Caspase-3 were observed by immunohistochemistry. Results Compared with model group, the cell apoptosis rates and the the expression of apoptosis-related protein Bax/Bcl-2 and Caspase-3 were decreased in different degree treated with SNX. The oxidation/anti-oxidation balance can be adjusted by SNX administration, serum SOD/MDA and NO/ET were increased than the model group (P<0.05、0.01). Conclusion SNX showed therapeutic benefits on rats in acute late-stage of cerebral ischemia injury.The potential mechanism of may be related to balance status of oxidation and anti-oxidation,Vasoactive substance, Bax/Bcl-2 ratio, and alleviating the expression Caspase-3, ultimately inhibit cell apoptosis.

R965

天津市第二批特支計(jì)劃青年拔尖人才基金（TJTZJHQNBJRC-2-7）