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体外培育牛黄对缺氧小鼠脑和心肌细胞的保护作用

The protective effects of in vitro cultivated calculus bovis on the cerebral and myocardial cells in hypoxic mice.

作者信息

Cai Hongjiao, Guang Yang, Liu Liegang

机构信息

Department of Surgery, Huazhong University of Science and Technology, Wuhan, 430030, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2007 Dec;27(6):635-8. doi: 10.1007/s11596-007-0603-2.

Abstract

The protective effects of in vitro cultivated calculus bovis (ICCB) on the cerebral and myocardial cells in hypoxic mice and the mechanism were examined. In one group, mice were intragastrically (i.g.) given ICCB for 15 days and then they were subjected to acute cerebral ischemia by decapitation, and then the panting time was recorded. In the other group, 12 min after exposure to hypoxia, mice was administered the ICCB i.g. for 5 days, and then the blood serum and tissues of brain, heart, liver were harvested and examined for SOD, GSH-px and T-AOC activity and content of MDA. The tissues of brain and heart were observed electron-microscopically for ultrastructural changes. The corpus striatum and hippocampus of brain were collected and examined for content of dopamine (DA) and norepinephrine (NE). The ultrastructural examination showed that the pathological change in brain and heart in the ICCB group was very slight, while abnormal changes in the control group were obviously more serious. ICCB significantly prolonged the panting time of the hypoxic mice (P<0.001), increased the activity of SOD, GSH-px, T-AOC in serum and tissues of brain, liver, heart and elevated the content of DA and NE. ICCB also pronouncedly reduced content of MDA in serum and tissues of brain, heart and liver. Significant differences in these parameters were noted between ICCB group and controls. It is concluded that ICCB can exert protective effect on the cells of brain and myocardium by enhancing the tolerance of the tissues to hypoxia and the body's ability to remove free radicals and regulating the neurotransmitters.

摘要

考察了体外培育牛黄(ICCB)对缺氧小鼠脑和心肌细胞的保护作用及其机制。一组小鼠灌胃给予ICCB 15天,然后通过断头使其遭受急性脑缺血,记录喘息时间。另一组小鼠缺氧暴露12分钟后,灌胃给予ICCB 5天,然后采集血清以及脑、心、肝组织,检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-px)、总抗氧化能力(T-AOC)活性以及丙二醛(MDA)含量。对脑和心脏组织进行电镜观察超微结构变化。采集脑的纹状体和海马检测多巴胺(DA)和去甲肾上腺素(NE)含量。超微结构检查显示,ICCB组脑和心脏的病理变化非常轻微,而对照组的异常变化明显更严重。ICCB显著延长了缺氧小鼠的喘息时间(P<0.001),增加了血清以及脑、肝、心脏组织中SOD、GSH-px、T-AOC的活性,提高了DA和NE的含量。ICCB还显著降低了血清以及脑、心、肝组织中MDA的含量。ICCB组与对照组在这些参数上存在显著差异。结论是,ICCB可通过增强组织对缺氧的耐受性、机体清除自由基的能力以及调节神经递质,对脑和心肌细胞发挥保护作用。

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