淫羊藿苷对神经细胞缺血再灌注损害的保护作用及其机制研究

Protective effect and its mechanism of Icariin on ischemia-reperfusion injury of neurons

目的探讨淫羊藿苷对神经细胞缺血再灌注损害的保护作用及其机制。方法对胎鼠脑皮质原代培养的神经元进行缺糖缺氧(OGD)和复糖复氧,制作拟缺血再灌注损害细胞模型;在OGD和复糖复氧时分别给予低、中、高剂量的淫羊藿苷干预。于复糖复氧24 h后检测细胞生存率、细胞外液乳酸脱氢酶(LDH)和细胞活性氧(ROS)水平。并与OGD模型组进行比较。结果各淫羊藿苷剂量组的细胞存活率均明显高于OGD模型组(P<0.05～0.01);淫羊藿苷中、高剂量组的细胞存活率又明显高于低剂量组(均P<0.05);中、高剂量组间细胞存活率的差异无统计学意义。各淫羊藿苷剂量组细胞外液LDH及细胞ROS水平均明显低于OGD模型组(P<0.05～0.01),淫羊藿苷中、高剂量组这两项指标的水平又明显低于低剂量组(P<0.05),中、高剂量组之间两项指标的差异无统计学意义。结论淫羊藿苷对神经细胞的缺血再灌注损害有保护作用,尤其以中、高剂量显著。其机制可能是通过抑制ROS的产生,减轻氧化应激损伤实现的。

Objective To investigate the protective effect and its mechanism of Icariin on ischemia-repeffusion injury of neurons. Methods The primary cultured cerebral cortical neurons of fetal mice were deprived of oxygen and glucose （OGD） which were then reintroduced imitating the cerebral isehemia-repeffusion injury. The low, middle and high-dose of Iearrin were added at the time of OGD and reintroduced. The survival rate of neuronal and the level of the lactate dehydrogenase （LDH） and reactive oxygen species （ROS） were determined after 24 h of reintroduction. And which were compared with OGD group. Results The survival rates of neuronal in the different dose Ieariin groups were significantly higher than that in the OGD group （ P 〈 0. 05 - 0.01 ）. The survival rates of neuronals in the middle and high-dose groups were obviously higher than that in the low-dose group（ all P 〈 0. 05 ）. There was no difference of the neuronal survival rates between the middle and high-dose groups. The levels of LDH and ROS in all Icarrin groups were significantly lower than those in the OGD group（P 〈0. 05 -0.01 ）. The levels of LDH and ROS in the middle and high-dose groups were obviously lower than that in the low-dose group（ P 〈 0. 05 ）. There was no difference of the two indexes between the middle and high-dose groups. Conclusions Icariin has a protective effects on the neurons with ischemia-repeffusion injury, which is more obviouse with middle and high-dose. The mechanism may carried out by suppressing ROS production and reducing the injury of oxidation stress.