藤茶总黄酮对大鼠脑缺血再灌损伤的保护作用

目的 探讨藤茶总黄酮对大鼠脑缺血后再灌注损伤的保护作用以及可能的作用机制。方法 阻断大鼠大脑中动脉血流制备大鼠脑缺血模型。96只Wistar大鼠，随机分为假手术组、模型对照组、阳性药组、藤茶总黄酮高、中、低剂量组。阳性药组以尼莫地平注射液10 mg·kg^-1·d^-1腹腔注射，藤茶总黄酮高、中、低剂量组分别以80，40，20 mg·kg^-1·d^-1灌胃给药，模型组和假手术组给予相同体积的生理盐水，每天1次，术前5 d开始给药。给药动物脑缺血2 h后再灌注24 h，处死动物。观察脑缺血大鼠神经行为学；TTC染色计算大鼠脑梗死面积；测定脑组织中SOD活性、MDA含量。结果 与模型组相比，藤茶总黄酮高、中剂量组均能减少梗死面积（P〈0.05），且大脑SOD活力显著升高（P〈0.05），MDA含量显著降低（P〈0.05）。结论 藤茶总黄酮对大鼠局灶性脑缺血损伤具有保护作用，其机制可能与抗氧自由基损伤有关。

Protective Effects of Tengcha Flavonoids on the Global Cerebral Ischemia Reperfusion Injury of Rats

OBJECTIVE To study the protective effects and mechanism of Tengcha flavonoids(TCF) on focal cerebral ischemia reperfusion injury in rats. METHODS Ninety-six Wistar rats were randomly divided into sham group, model group, nimodipine group(10 mg·kg^-1·d^-1, TCF low dose, middle dose, high dose group(20, 40 and 80 mg·kg^-1·d^-1). Control group and model group were given the same volume of physiological saline, once a day, for gavage 5 days. Cerebral ischemia model was established in rats through occluding the middle cerebral artery (MCAO). After ischemia for 2 h, all animals were reperfused for 24 h and were killed. Behavior and infarct size were evaluated, and malondi-aldehyde(MDA) content and superoxide dismutase(SOD) activity of brain were observed. RESULTS Compared with the model group, the infarction area in the TCF 40 and 80 mg·kg^-1·d^-1 groups were significantly lower(P<0.05), MDA content of brain tissue of all TCF groups decreased(P<0.05) and SOD activity increased significantly(P<0.05). CONCLUSION TCF have protective effects on focal brain ischemia reperfusion injury in rats by improving state of oxidative stress and increasing activity of antioxidant enzymes.