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目的研究补阳还五汤预处理对局灶性脑缺血再灌注损伤大鼠磷酸化丝氨酸/苏氨酸蛋白激酶(p-Akt)及Akt的影响,并探讨其作用机制。方法将SD大鼠100只,随机分成5组(每组20只):假手术组,模型组,硫酸氢氯吡格雷组(6.8 mg·kg-1),补阳还五汤高、低剂量组(26,13 g·kg-1)。采用改良线栓法复制大鼠大脑中动脉栓塞(MCAO)再灌注模型。脑缺血1 h再灌注6 h后进行神经功能缺失评分;氯化三苯基四氮唑(TTC)染色法检测脑梗死面积;苏木精-伊红(HE)染色法观察海马区神经细胞形态变化;免疫印迹法(Western blot)检测海马区p-Akt和Akt蛋白表达量的变化情况。结果与假手术组比较,模型组的神经功能缺失评分显著升高(P<0.01),说明造模成功;与模型组比较,补阳还五汤高、低剂量组和硫酸氢氯吡格雷组能不同程度地改善MCAO再灌注大鼠的神经功能缺失症状(P<0.05,P<0.01),降低海马区神经细胞的损伤程度,缩小脑梗死面积(P<0.05,P<0.01),促进p-Akt的表达(P<0.05)。结论补阳还五汤对脑缺血再灌注大鼠的脑损伤具有一定的的预防和保护作用,其作用机制可能与提高Akt磷酸化的水平有关。
Objective To investigate the effect of Buyang Huanwu Decoction preconditioning on phosphorylated serine / threonine protein kinase (p-Akt) and Akt in focal cerebral ischemia-reperfusion injury rats and its mechanism. Methods 100 SD rats were randomly divided into 5 groups (20 in each group): sham operation group, model group, clopidogrel hydrogen sulfate group (6.8 mg · kg-1), Buyang Huanwu Decoction high and low dose Group (26, 13 g · kg -1). Rat model of middle cerebral artery occlusion (MCAO) reperfusion was reproduced by modified thread method. Neurological deficit scores were measured at 1 h after cerebral ischemia and 6 h after reperfusion. Cerebral infarction area was detected by TTC staining. Hematoxylin and eosin (HE) The changes of p-Akt and Akt protein expression in hippocampus were detected by Western blot. Results Compared with the sham operation group, the score of neurological deficit in the model group was significantly increased (P <0.01), indicating that the model was successful. Compared with the model group, BYHWD high and low dose group and clopidogrel hydrogen sulfate group (P <0.05, P <0.01), reduce the damage of hippocampal nerve cells, reduce the area of cerebral infarction (P <0.05, P <0.01) and promote the expression of p -Akt expression (P <0.05). Conclusion Buyang Huanwu decoction can prevent and protect brain injury induced by cerebral ischemia and reperfusion in rats. The mechanism may be related to the increase of Akt phosphorylation.