硒对铅暴露致神经损伤的拮抗作用研究

目的:研究铅暴露诱导的神经毒性损伤作用,明确铅暴露引发神经毒性损伤的部分机制以及硒的保护作用。方法:通过哺乳期染铅及补充硒建立铅暴露动物模型;通过TUNEL实验确定铅暴露引发的神经损伤;通过Western blot实验检测Bax、Bcl-2、Caspase-3水平确定铅暴露对凋亡途径的启动;并确证补硒在铅神经毒性作用下对机体的保护作用。结果:1.哺乳期铅暴露能够引起仔鼠海马神经细胞凋亡的发生;2.铅暴露能够诱导Bax/Bcl-2水平改变,激活Caspase-3。3.同时给予硒干预后,机体抗铅神经毒性能力显著增加。结论:1.铅暴露能够诱导海马部位神经毒性损伤,损伤可能通过启动凋亡途径而发生,2.补硒能够通过拮抗凋亡发生从而拮抗铅的神经毒性,产生保护作用。

The Effect of SeleniumSupplementary on Lead Induced Neurotoxicity

Objective:To investigate the effect of lead exposure on neurotoxicity, and to identify the mechanism of lead exposure on neurotoxicity and clear protection effect of selenium supplementary.Methods:Establish the lead exposure and selenium supplementary animal model by lactation lead exposure and supplementary with selenium. The damage caused by the lead on the hippocampal neurons were detected by in situ TUNEL assay. The activity of apoptosis-related proteins was detected by Western blot; The protective effect of selenium supplementary in lead neurotoxicity was also confirmed.Results:1. Lactating lead exposure could induce hippocampal neuronal apoptosis; 2. Lead exposure could alter the expression of apoptosis-related proteins such as Bax, Bcl-2 and Caspase-3. 3. Selenium supplementary could alleviate lead neurotoxicity.Conclusion:1. Lead exposure could induce hippocampal neuronal injury and this injury may trigger by apoptosis pathway; 2. Selenium supplementary may resist lead induced apoptosis thereby protect neurons fromlead neurotoxicity.