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作 者:涂建锋[1] 魏良浩[1] 周晟昂[1] 张可[1] 陈环[1] 张美齐[1] 蔡文伟[1] 杨悦[2]
机构地区:[1]浙江省人民医院急诊医学科,杭州310014 [2]浙江医学高等专科学校,杭州310053
出 处:《中华中医药杂志》2015年第11期4141-4144,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:浙江省中医药科学研究基金计划资助项目(No.2010ZA003);浙江省科技厅公益性技术应用研究计划实验动物平台项目(No.2013C37022)~~
摘 要:目的:探讨补阳还五汤对脑缺血再灌注大鼠海马CA4区Hes-1和Hes-5表达的影响。方法:63只SD大鼠随机分为补阳还五汤(BYHWT)组、脑缺血再灌注损伤模型(I/R)组和假手术(Sham)组3组。大脑中动脉阻塞线栓(MCAO)法建立局灶性脑缺血再灌注大鼠模型。脑缺血2h后再灌注10、19和28d,显微镜观察阳性细胞形态特点,免疫组化法检测CA4区Hes-1和Hes-5阳性细胞数目。结果:10d和19d BYHWT亚组Hes-1及Hes-5阳性细胞数目分别高于I/R和Sham组(P<0.01);28d BYHWT亚组显著低于I/R与Sham组(P<0.01)。I/R和BYHWT的19d亚组分别高于其对应的10d亚组(P<0.01)。结论:补阳还五汤在脑缺血再灌注损伤早中期通过上调海马CA4区Hes-1和Hes-5表达,晚期通过下调其表达,从而对局灶性脑缺血再灌注损伤产生神经修复作用。Objective: To investigate the effects of Buyang Huanwu Decoction(BYHWT decoction) on the expressions of Hes-1 and Hes-5 in the hippocampus CA4 of rats with focal cerebral ischemic-reperfusion(I/R) injury. Methods: Sixty-three SD rats were randomly divided into BYHWT group, cerebral I/R injury model(CIRI) group and sham group. The method of middle cerebral artery occlusion(MCAO) was performed to establish the focal cerebral I/R injury model. Each 7 rats in one group were respectively reperfused 10 days, 19 days and 28 days after two hours cerebral ischemic. Then, the immunohistochemical technique was used to observe the morphological characteristics and numbers of Hes-1 and Hes-5 positive cells. Results: The positive cell numbers in BYHWT group following 10 days and 19 days reperfusion were significant higher than those in both CIRI group and sham group(P〈0.01), but BYHWT group following 28 days was significant lower than those in both CIRI group and Sham group(P〈0.01). And, the positive cell numbers in BYHWT group and CIRI group following 19 days reperfusion were both significant higher than those in BYHWT group and CIRI group following 10 days reperfusion(P〈0.01). Conclusion: BYHWT Decoction could have an effect of neural repair on focal cerebral I/R injury, the mechanism of which might be related to up-regulation the expressions of Hes-1 and Hes-5 during the early and middle phase and down-regulation in the late phase in hippocampus CA4.
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