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作 者:陈李芳[1] 冯宏业[1] 李竞[1] 韩漫夫[1]
机构地区:[1]深圳市第二人民医院神经内科,广东深圳518035
出 处:《中风与神经疾病杂志》2012年第3期262-265,共4页Journal of Apoplexy and Nervous Diseases
基 金:深圳市科技计划基金资助项目(编号200802040)
摘 要:目的研究p38MAPK通路抑制剂SB203580在液化石油气中毒大鼠模型中对神经元的保护作用。方法采用大鼠液化石油气中毒模型,72只SD大鼠随机分为正常对照组、中毒组和SB203580干预组,干预组在中毒前1h腹腔注射SB203580(10mg/kg,溶于5mg/ml DMSO),动物分别于中毒后1d、3d、7d处死,观察脑组织神经元的形态变化,免疫组化方法检测脑组织p38MAPK的表达水平。结果中毒组大鼠脑组织神经元坏死,p-p38MAPK阳性细胞大量表达,干预组大鼠上述变化明显减轻(P<0.05)。结论在液化石油气中毒大鼠模型中,SB203580通过抑制p38MAPK通路减少神经元坏死,发挥神经保护作用。Objective To investigate the protective effect of SB203580 on neurons in rats after acute liquid petroleum gas (LPG)poisoning. Methods Liquid petroleum gas poisoning model rats was established. SD rats were randomly divided into three groups:model group, poisoning group and inhibitor group. Inhibitor group were treated with SB203580 (10mg/kg,dissolved in 5mg/ml DMSO ,intraperitoneal injection)lh before poisoning. The rats were killed respectively on ld,3d,Td 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 neuronal necrosis was observed in LPG treated rats, and p-p38MAPK positive cells increased significantly compared with those in control group( P 〈 0.05 ). In inhibitor group,those changes were reduced obviously (P 〈 0.05). Conchlsion SB203580 decreases LPG-induced neuronal necrosis in rat brain by inhibiting P38MAPK and plays a neuroprotective role in LPG poisoning model rats.
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