补肾益气方对大脑中动脉闭塞大鼠PI3K/AKT通路的影响  

Effects of Bushen Yiqi Formula on PI3K/AKT pathway in middle cerebral artery occlusion rats

作　　者：刘爱华 孙婧 孔令雯 韩振翔[2] 董竞成 LIU Ai-hua;SUN Jing;KONG Ling-wen;HAN Zhen-xiang;DONG Jing-cheng(Department of Integrative Medicine,Huashan Hospital Affiliated to Fudan University,Shanghai 200040,China;Department of Neurological Rehabilitation,Seventh People's Hospital of Shanghai University of TCM,Shanghai 200137,China)

机构地区：[1]复旦大学附属华山医院中西医结合科,上海200040 [2]上海中医药大学附属第七人民医院神经康复科,上海200137

出　　处：《中华中医药杂志》2022年第9期5329-5333,共5页China Journal of Traditional Chinese Medicine and Pharmacy

基　　金：国家自然科学基金项目(No.81703997);国家中医药管理局“第六批全国老中医药学术经验继承工作”项目(No.国中医药人教发[2017]29号)。

摘　　要：目的:明确补肾益气方对大鼠大脑中动脉缺血再灌注损伤模型的神经保护作用,进一步探讨其机制是否与PI3K/AKT信号通路有关。方法:42只SD大鼠随机分为假手术组,模型组,补肾益气颗粒低、中、高剂量(0.6、3、6 g)组,阿加曲班组,LY294002组,每组6只。假手术组仅行游离血管操作,不做插线处理,余各组采用Zea Longa大脑中动脉线栓法构建大脑中动脉闭塞(MCAO)大鼠模型,缺血90 min,再灌注24 h后,进行神经功能缺损评分测定,采用四唑染色法(TTC)测定脑梗死体积,尼氏染色法评估脑细胞损伤程度,免疫印迹法测定大鼠脑片(缺血侧基底节)组织中p-AKT、AKT的表达。结果:与假手术组比较,其余各组大鼠神经功能缺损评分显著升高(P<0.01);模型组、阿加曲班组、LY294002组脑梗死体积比显著增加(P<0.01,P<0.05);其余各组完整细胞数显著减少(P<0.01);模型组与LY294002组p-AKT/AKT表达水平显著降低(P<0.01)。与模型组比较,补肾益气颗粒中、高剂量组与阿加曲班组大鼠神经功能缺损评分显著降低(P<0.05,P<0.01);补肾益气颗粒高剂量组及阿加曲班组脑梗死体积比显著减少(P<0.01,P<0.05);补肾益气颗粒高剂量组及阿加曲班组完整细胞数显著增加(P<0.01,P<0.05);补肾益气颗粒中、高剂量组及阿加曲班组的p-AKT/AKT表达水平显著上升(P<0.05,P<0.01)。结论:补肾益气颗粒可有效减轻大鼠脑缺血再灌注损伤,其神经保护作用机制可能与通过激活PI3K/AKT信号通路有关,其疗效与阿加曲班相当。Objective: To investigate the neuroprotective effect of Bushen Yiqi Formula on middle cerebral artery ischemia-reperfusion injury model in rats, and further explore whether the mechanism is related to the PI3K/AKT signaling pathway. Methods: Forty-two SD rats were randomly divided into 7 groups, namely sham operation group, model group, low-, medium-, high does BSYQ Granules(0.6, 3, 6 g) groups, argatroban group and LY294002 group, 6 rats in each group. The rats in the sham operation group were given only isolating middle cerebral artery, and no inserting thread operation, and the rats in the other groups were induced into middle cerebral artery occlusion(MCAO) model by Zea Longa method. After ischemia for 90 min and reperfusion for 24 h, the neurological deficit scores were calculated, the volume of cerebral infarction was measured by tetrazole staining(TTC), the degree of brain cell injury was assessed by Nissl staining, and the expression of p-AKT and AKT in the ischemic basal ganglia of rats was determined by Western Blot. Results: Compared with the sham operation group,the neurological deficit scores of rats in the other groups were increased(P<0.01), the ratio of infarct volume in model group,argatroban group and LY294002 group was significantly increased(P<0.01, P<0.05), the number of intact cells in the other groups was significantly decreased(P<0.01);the p-AKT/AKT expression level in the model group and LY294002 group was significantly decreased(P<0.01). Compared with the model group, the neurological function deficit scores of rats in the medium-,high-dose BSYQ Granules groups and the argatroban group were significantly decreased(P<0.05, P<0.01);the ratio of infarct volume in the high-dose BSYQ Granules group and the argatroban group were significantly decreased(P<0.01, P<0.05);the number of intact cells in the high-dose BSYQ granules group and argatroban group increased significantly(P<0.01, P<0.05);the expression level of p-AKT/AKT increased in medium-, high-dose BSYQ Granules groups and argatroban gr

关 键 词：补肾益气方 脑缺血再灌注损伤 PI3K/AKT信号通路 神经保护 中动脉闭塞 

分 类 号：R285.5[医药卫生—中药学]