液化石油气中毒大鼠脑组织p38MAPK的表达及意义研究  

Expression and Significance of p38MAPK in Brain of Rats with Liquid Petroleum Gas Poisoning

作　　者：陈李芳[1] 李竞[1] 韩漫夫[1] 

机构地区：[1]广东省深圳市第二人民医院神经内科,518035

出　　处：《临床合理用药杂志》2011年第05X期17-19,共3页Chinese Journal of Clinical Rational Drug Use

基　　金：深圳市科技计划基金资助项目(200802040)

摘　　要：目的观察p38MAPK在液化气中毒大鼠脑组织中的表达,探讨p38MAPK信号通路在液化气中毒大鼠发病中的作用。方法采用大鼠液化石油气中毒模型,动物分别于中毒后1、3、7d处死,苏木精-伊红染色观察脑组织神经细胞的形态变化,免疫组化方法检测脑组织p38MAPK的表达水平。结果大鼠液化石油气中毒后大脑皮质神经元细胞核浓缩、结构不清,可见神经元坏死迹象。免疫组化技术观察显示p38MAPK在急性液化气中毒大鼠脑组织中的表达与正常组比较明显增加,差异有统计学意义(P<0.05)。结论 p38MAPK信号传递途径促进液化石油气中毒诱导的大鼠脑组织神经元坏死,在液化石油气中毒大鼠发病中起重要作用。Objective To evaluate the expression levels of p38MAPK in rats after acute liquid petroleum gas poisoning （ALPGT） and explore the functional mechanism of p38MAPK in the pathological changes of ALPGT. Methods Liquid petroleum gas poisoning model rats was established, the rats were killed respectively 1, 3, 7 days after poisoning, the morphological changes in neuron were observed by HE staining. The expression levels of p38MAPK in brain was detected by using immunohistochemistry. Results The degeneration of neurons and inspissation of karyon were observed in LPG treated rats; and the expression of p38MAPK in brain of rats after ALPGT increased significantly compared with those the control group （ P 〈 0. 05 ）. Conelusion P38MAPK contributes to LPG - induced neuronal necrosis in rat brain and play an important role in ALPGT.

关 键 词：液化石油气中毒 神经元 P38MAPK 

分 类 号：R595.1[医药卫生—内科学]