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作 者:李新娟[1] 葛治国[2] 李东亮[1] 李庆岗[3] 李明阳[3] 秦宇[3] 赵明虎[3]
机构地区:[1]新乡医学院生理学与神经生物学教研室,河南新乡453003 [2]新乡医学院基础医学院,河南新乡453003 [3]新乡医学院,本科2003级河南新乡453003
出 处:《新乡医学院学报》2006年第6期569-571,共3页Journal of Xinxiang Medical University
摘 要:目的观察牛磺酸(Tau)对弥漫性颅脑损伤大鼠学习记忆和海马Bcl-2和Bax蛋白表达的影响,探讨其神经保护作用机制。方法Marmarou方法建立大鼠弥漫性颅脑损伤模型,Y型迷宫检测大鼠认知功能,免疫组织化学方法检测脑组织海马区Bcl-2和Bax蛋白表达的变化。结果低、中、高剂量Tau组的记忆成绩均明显高于损伤组(P<0.01)。中、高剂量Tau组海马区Bcl-2蛋白表达均明显多于损伤组(P<0.01);Bax蛋白表达均明显少于损伤组(P<0.01);Bcl-2/Bax表达比均明显高于损伤组(P<0.01)。结论促进海马上调Bcl-2蛋白表达、下调Bax蛋白表达、调节Bcl-2/Bax比、抑制神经细胞凋亡可能是Tau对抗损伤保护脑的一种途径。Objective To investigate the neuroprotective mechanism of taurine(Tau) by observation of the effects Tau on the cognitive function and the expression of Bcl-2 and Bax at hippocampus after diffuse brain injury(DBI) in rats. Methods The model of DBI was established according to the method created by Marmarou. The cognitive function was observed by Y- type maze before and 24h after DBI in rats respectively. Immunohistochemistry staining was used to examine the expression of Bcl-2 and Bax in hippocampus. Results The cognitive function was significantly improved in the lower, middle and high dose Tau groups compared with simple DBI group(P〈 0.01 ). The amount of the positive cell of Bcl-2 in high and middle dose group significantly increased compared with simple DBI group(P〈0.01)and the amount of the positive cell of Bax in high dose and middle dose group significantly decreased compared with simple DBI group( P〈 0.01 ). At the same time Bcl-2/Bax expression ratio in high and middle dose group significantly increased compared with simple DBI group( P 〈 0.01 ). Conclusion It may be a way of cerebroprotective effect that Tau protects nerve cell from apoptosis by promoting the expression of Bcl-2, reducing the expression of Bax and adjusting the ratio of Bcl-2/Bax.
关 键 词:脑损伤 牛磺酸 BCL-2 BAX 学习记忆 大鼠
分 类 号:R743[医药卫生—神经病学与精神病学]
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