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染料木素对实验性脑出血大鼠PI3K/Akt通路的影响 被引量:3

Effects of genistein on PI3K/Akt pathway in cerebral hemorrhage rats
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摘要 目的:探讨染料木素对实验性脑出血(intracerebral hemorrhage,ICH)大鼠神经功能损伤的保护作用及相关的作用机制。方法:随机将大鼠分为假手术组、ICH模型组、染料木素低剂量组(5 mg/kg)、中剂量组(10 mg/kg)和高剂量组(15 mg/kg)。通过注射IV型胶原酶建立ICH大鼠模型,采用Garcia法对大鼠进行神经功能缺损评分,湿重法检测脑含水量,比色法检测脑组织中SOD与过氧化氢酶(catalase,CAT)的含量水平,TUNEL法检测血肿周围脑组织细胞凋亡数,Western印迹法检测脑组织中p-PI3K与p-Akt蛋白表达水平。结果:与ICH模型组相比,染料木素给药后,大鼠的神经功能缺损评分显著升高,脑含水量明显下降,脑组织中SOD与CAT的含量水平升高,血肿周围脑组织的细胞凋亡数降低,p-PI3K与p-Akt的蛋白表达明显上调。结论:染料木素对ICH后的脑损伤具有一定的保护作用,可能与染料木素的抗氧化作用及调控PI3K/Akt通路有关。 Objective: To investigate the protective effects of genistein on neuronal function in cerebral hemorrhage rats and explore the underlying mechanisms. Methods: Rats were randomly divided into the following groups: a sham group, a model group, and cerebral hemorrhage rats treated with low, medium or high dose of genistein groups. Cerebral hemorrhage rat model was induced by injection of type IV collagenase. Neuronal functions were determined by Garcia method; the brain water content(BWC) was measured by wet weight method; SOD and catalase(CAT) levels in brain tissue were examined with colorimetric method; cell apoptosis was observed by TUNEL staining, and the expressions of p-PI3 K and p-AKT were detected by Western blot. Results: Compared with the model group, neuronal function was significantly improved after genistein treatment. Moreover, the BWC and cell apoptosis in the brain were decreased, while the levels of SOD and CAT, and the expression of p-PI3 K and p-AKT were increased after genistein treatment. Conclusion: Genistein can improve neuronal function in cerebral hemorrhage rats, which may be associated with its anti-oxidative effects and regulation of PI3 K/Akt pathway.
作者 吴环立 马现启 赵海洋 WU Huanli;MA Xianqi;ZHAO Haiyang(Department of Neurosurgery, Second General Hospital of Nanyang, Nanyang He'nan 473000, Chin)
出处 《临床与病理杂志》 2018年第5期917-921,共5页 Journal of Clinical and Pathological Research
关键词 染料木素 脑出血 抗氧化 PI3K/AKT genistein cerebral hemorrhage anti-oxidative effect PI3K/Akt
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