氯菊酯诱导脑源性神经生长因子的表达
Expression of nerve growth factor induced by permethrin treatments
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摘要:目的 为了进一步阐明氯菊酯(PM)的神经毒作用机制。方法 用逆转录-PCR(RT-PCR)、斑点杂交、流式细胞仪及免疫组织化学技术检测了氯菊酯对大鼠脑组织中脑源性神经生长因子(BDNF)表达的影响。结果 大鼠一次大剂量〔PM1, 400mg/(kg°d), ip〕或反复小剂量〔PM2, 200mg/(kg°d), ip〕给予氯菊酯后, 明显诱导其大脑皮层和海马的BDNFmRNA水平: RT-PCR表明PM1和PM2组大鼠皮层和海马BDNFmRNA诱导率分别为67%, 81%和53%和54%。斑点杂交亦显示, PM1和PM2组皮层和海马BDNF的水平分别高出对照组57%, 78%和36%, 50%, 且均表现为对皮层的诱导强于海马。而BDNF蛋白表达结果表明, 氯菊酯对蛋白水平的影响与BDNFmRNA并不一致: 流式细胞分析表明PM1和PM2组大鼠皮层BDNF的蛋白表达均明显升高, 尤其是PM2组, 其BONF蛋白水平是对照组的237%, 然而海马BDNF蛋白量无明显改变; 免疫组化结果与流式细胞分析基本一致, 仅PM1组海马CA1区蛋白表达较对照组高21%。结论 氯菊酯诱导大脑皮层和海马BDNF的表达可能在其神经损伤修复中有重要意义。Abstract:Objective To elucidate the mechanism of per methrin on central nervous system(CNS).Methods The levels of brain-derived neurotrophic factor(BDNF)mRNA and protein expression in ratcor tex and hippocampus were examined by RT-PCR, dot blot, flow cytometry analysis and immunochemistry.Results RT-PCR and dot blot analysis indicated the levels of BDNFmRNF expression in rat brain were up-regulated by permethrin(PM)administration at a high dose(PM1, 400mg/kg°d, ip)one times and a low dose(PM2, 200mg/kg°d, ip)for 5 days, especially in cortex.However the protein expression of BDNF was not correspond to the level of BDNF mRNA: in spite of marked increase of BDNF protein expression of rat cortex in PM1 and PM2 groups were observed by flow cytometry analysis and immunochemistry, the levels of BDNF protein in rathippocampus remained unchanged except CA1 region in PM1 group.Conclusion The involvement of induction of BDNF expression in ratbrain may play a role in neur oprotective profiles of CNS injury.
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