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【目的】 研究即早基因 (IEG)在氯化甲基汞神经毒性机制中的作用。【方法】 应用Fos和Jun蛋白免疫组织化学方法 ,对腹腔注射氯化甲基汞 (0 6mg/kg及 6 0mg/kg)的大鼠不同脑区c fos、c jun表达水平进行观察。【结果】 经图像分析及统计检验结果显示 ,急性染汞 2h后 ,大鼠脑组织皮层、海马CA3 区及小脑的Fos、Jun表达的阳性面积比 [Aa(% ) ]、平均灰度和阳性细胞个数 (n) 3个参数与对照组相比 ,差异有显著性 (P <0 0 5 ) ,即染汞组IEG表达高于对照组。例如 :高剂量组、低剂量组和对照组在海马CA3 区的Fos表达的平均灰度分别为 136± 8,149± 14,178± 15。【结论】 提示第三信使IEG作为转录调控因子参与了氯化甲基汞对中枢神经损害的毒性过程。这对深入阐明汞神经毒性的分子机制提供了一定的实验依据。并建议将IEG作为氯化甲基汞神经毒性检测和评价的效应指标
【Objective】 To investigate the role of early gene (IEG) in the mechanism of methylmercury chloride neurotoxicity. 【Methods】 The expressions of c fos and c jun in different brain regions of rats injected intraperitoneally with Methylmercury Chloride (0 6 mg / kg and 60 mg / kg) were observed by Fos and Jun protein immunohistochemistry. 【Result】 The results of image analysis and statistical tests showed that the positive area ratio (Aa (%)], average grayscale and positive expression of Fos and Jun in cerebral cortex, hippocampal CA3 and cerebellum The number of cells (n) 3 parameters compared with the control group, the difference was significant (P <0 05), that is, mercury staining IEG expression was higher than the control group. For example, the average gray level of Fos expression in high dose group, low dose group and control group in hippocampal CA3 region were 136 ± 8,149 ± 14,178 ± 15 respectively. 【Conclusion】 The third messenger IEG is suggested as a transcriptional regulator involved in the toxicity of methylmercury chloride to central nervous system damage. This provides some experimental evidence for further elucidating the molecular mechanism of mercury neurotoxicity. IEG is recommended as an indicator of the effect of IEG on neurotoxicity testing and evaluation