细胞凋亡在热打击致大鼠大脑皮质神经元损害中的作用及机制

Role of cell apoptosis in neuronal injury in rat cerebral cortex induced by heat stress and related mechanisms

摘要:

目的 探讨热打击后大鼠大脑皮质神经元凋亡及caspase-3的表达变化。方法 将Wistar大鼠随机分为正常对照组和热打击组，正常对照组大鼠始终置于（25±0.5）℃，相对湿度（35±5）%环境下；热打击组置于人工智能气候舱内100 min，舱内温度（40±0.5）℃，相对湿度（60±5）%。TUNEL染色观察大鼠大脑皮质神经元的凋亡情况；免疫组织化学方法及荧光定量PCR检测大鼠大脑皮质神经元caspase-3的表达。结果 热打击1 d后大脑皮质神经元出现凋亡，第3天达高峰。caspase-3于热打击2 d后开始表达，于第3天表达最明显。荧光定量PCR检测结果显示，caspase-3在1 d、2 d、3 d和7d各时间点含量与正常对照组比较差异均有统计学意义（P<0.05），3 d时caspase-3含量最高。结论 热打击可激活caspase-3表达，诱导皮质神经元凋亡。

Abstract:

Objective To investigate the apoptosis of neurons and the change in the expression of caspase-3 in rat cerebral cortex induced by heat stress.Methods Wistar rats were randomly divided into normal control group and heat stress group. The rats in the normal control group were placed in an environment with a temperature of (25±0.5)℃ and a relative humidity of 35%±5%, and those in the heat stress group were placed in a chamber with a temperature of (40±0.5)℃ and a relative humidity of 60%±5% for 100 minutes. TUNEL staining was used to observe the apoptosis of neurons in rat cerebral cortex, and immunohistochemistry and quantitative real-time PCR were used to measure the expression of caspase-3 in neurons.Results The apoptosis of cerebral cortex neurons appeared at 1 day after heat stress and reached the peak at 3 days. Caspase-3 expression appeared at 2 days after heat stress and reached its peak at 3 days. Quantitative real-time PCR showed that there was a significant difference in the content of caspase-3 at 1, 2, 3, and 7 days between the heat stress group and the normal control group, and the heat stress group had the highest content of caspase-3 at 3 days.Conclusions Heat stress can activate the expression of caspase-3 and induce apoptosis of cerebral cortex neurons.