β-细辛醚对缺糖缺氧再灌注损伤原代大鼠海马神经元的保护作用*

 目的：探讨β-细辛醚对缺糖缺氧再灌注损伤原代海马神经元的保护作用及其机制。方法：利用MTT法检测缺糖缺氧再灌注诱导的原代大鼠海马神经元的细胞活力，用分光光度法检测caspase-3的活性，用Western blotting法检测p-JNK和Bcl-2的蛋白表达，RT-PCR检测Bcl-2和caspase-3 mRNA表达。结果：与正常对照组比较，缺糖缺氧再灌注损伤组细胞活力明显下降，caspase-3活性明显升高，p-JNK蛋白表达和caspases-3 mRNA表达显著升高，Bcl-2蛋白表达显著降低，差异有统计学意义（均P＜0.05）。与缺糖缺氧再灌注损伤组比较，不同剂量β-细辛醚预处理组抑制了这些指标的改变（均P＜0.05）。结论：β-细辛醚通过抑制JNK介导的线粒体通路抑制缺糖缺氧再灌注诱导的原代海马神经元凋亡。

Protective effect of β-asarone on primary rat hippcampal neurons against hypoxia/hypoglycemia and reperfusion injury

AIM：To investigate the protective effect of β-asarone against hypoxia/hypoglycemia and reperfusion injury in primary rat hippocampal neurons. METHODS：Cell viability, the activity of caspase-3, the protein expression of p-JNK and Bcl-2, and the mRNA expression of Bcl-2 and caspase-3 were determined by MTT assay, spectrophoto-metry, Western blotting and real-time PCR. RESULTS：Compared with normal control group, the cell viability decreased and the activity of caspase-3 increased obviously, the expression of p-JNK protein and caspase-3 mRNA increased obviously, and  the expression of Bcl-2 protein decreased obviously in model group (P<0.05). Compared with model group, different doses of β-asarone inhibited the changes of the above indexes (P<0.05). CONCLUSION：β-asarone inhibits JNK-mediated chondrosome signaling pathway, thereby attenuating the process of hippocampal neuron apoptosis after hypoxia/hypoglycemia and reperfusion.