丹参酮对原代大鼠海马神经元细胞缺氧缺糖损伤的保护作用

Protective effect of tanshinone against the damage to the hippocampus nerve cells in rats during oxygen-glucose deprivation.

目的观察缺氧缺糖对大鼠海马神经元细胞的影响及丹参酮的保护作用。方法取体外培养12天的海马神经元细胞随机分为正常对照组、缺氧缺糖组、丹参酮20μmol/L组、丹参酮40μmol/L组、丹参酮80μmol/L组(后3组缺氧缺糖前24h,加入丹参酮预处理)。缺氧缺糖组、各浓度丹参酮组在缺氧缺糖环境中培养2、4、24及36h后,收集其各个时间点的培养液,测定培养液中乳酸脱氢酶(LDH)含量。结果缺氧缺糖后,缺氧缺糖组各个时间点LDH渗出量明显高于正常对照组,经丹参酮预处理的神经元损伤有不同程度的减轻,各个时间点LDH渗出量明显低于对应的缺氧缺糖组。结论缺氧缺糖可引起海马神经元损伤,丹参酮对海马神经元细胞损伤具有保护作用。

Objective To investigate the damage of oxygen-glucose deprivation to the hippocampus nerve cells in rats and the protective effects of tanshione. Methods The hippocampus nerve cells were cultured in vitro for 12 days and randomly classified into control group, oxygen-glucose deprivation group and tanshinone-treated group. Twenty-four h before oxygen-glucose deprivation, the tanshinone （20, 40 and 80μmol/L） was added to the culture medium respectively in the tanshinone-treated group. The morphology of hippocampus never cells was observed and LDH was measured in the culture medium collected at 2, 4, 24 and 36 h after hypoxia in the oxygen-glucose deprivation group and tanshinone-treated group. Results After oxygen-glucose deprivation, LDH levels in the oxygen-glucose deprivation groups were increased as compared with the control group. In the tanshinone-treated group, the damage to the hippocampus nerve cells was aggravated and the LDH levels were decreased as compared with the oxygen-glucose deprivation group. Conclusion Oxygen-glucose deprivation could induce the damage to the hippocampus nerve cells and the tanshinone could provide protection against such damage.