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作 者:吕仁花[1] 索爱琴[2] 张杰文[2] 赵建华[2] 黄月[2]
机构地区:[1]新乡医学院,河南省新乡市453000 [2]河南省人民医院神经内科,郑州市450003
出 处:《实用诊断与治疗杂志》2007年第4期278-279,共2页Journal of Practical Diagnosis and Therapy
摘 要:目的:观察缺血预处理对大鼠原代培养神经元缺血耐受性的影响,并探讨缺血预处理对bcl-2表达的影响。方法:体外培养的原代神经元分为对照组和预处理组,对照组给予类缺血30 min复氧复糖培养24 h;预处理组经类缺血10 min预处理后复氧复糖培养24 h后,再给予致死性的类缺血30 min复氧复糖培养24 h,两组细胞均用TUNEL法检测神经元凋亡,并计算存活和凋亡神经元所占百分率。同时用免疫组化法观察两组细胞bcl-2的表达。结果:对照组神经元的凋亡率明显高于预处理组,对照组bcl-2的表达明显低于预处理组,差异有统计学意义。结论:缺血预处理能够诱导神经元的缺血耐受性,预处理可能通过激活bcl-2增加其表达发挥神经保护作用。Objective To study the effect of ischemic preconditioning on ischemic tolerance and the expression of bcl-2 in primary cultured rat cortical neurons. Methods The neurons primary cultured in vivo were randomly divided into control group treated with 30 minutes ischemia and ischemic preconditioning group treated with 10 minutes ischemic preconditioning before 30 rain ischemia. The apoptosis was detected with TUNEL. Bcl-2 expressions were studied with immunohistochemical assay. Results The apoptosis rate in control group was obviously higher than that in ischemic preconditioning group. The expression of bcl-2 in control group was obviously lower than that in ischemic preconditioning group. And there was a statistic difference between control group and ischemic preconditioning group. Conclusion Ischemic preconditioning can induce ischemic tolerance in cultured cortical neurons. Preconditioning might activate bcl-2 and improve its role of neuroprotection.
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