刺五加多糖的抗氧化损伤作用研究

摘要 目的：研究刺五加多糖（Acanthopanacis senticosi polysaccharides，ASPS）对大鼠海马细胞有无抗氧化损伤作用，并探讨其可能机制。方法：运用海马神经细胞原代培养技术，采用H2O2诱导建立细胞氧化损伤模型。观察细胞形态学变化；MTT法测定细胞活性；免疫组化法检测细胞中P53蛋白表达；检测细胞外液中的乳酸脱氢酶（LDH）的活力，细胞匀浆液中的过氧化物歧化酶（SOD），丙二醛（MDA）产生。结果：形态学观察显示：与模型组比较，ASPS组细胞损伤程度明显减轻；ASPS组细胞活性（0.46）比模型组细胞活性（0.36）高(P＜0.01) , ASPS组P53表达量较低而模型组表达量较高； LDH、NOS活力及MDA生成量ASPS组明显低于模型组，但SOD活力ASPS组显著高于模型组。结论：ASPS能提高海马神经细胞的抗氧化能力，并具有一定的浓度依赖性。

Study on the Effect of Antioxidative Damage by Acanthopanacis Senticosi Polysaccharides

Objective To study whether acanthopanacis senticosi polysaccharides (ASPS) has an antioxidative effect on the hippocampal neurons in rats and to explore its possible mechanisms. Methods The model of neuronal injury in the hippocampus was constructed by H2O2-induced oxidation. Changes in the morphology of the cell were observed. Activity of the hippocampal neurons was detected by MTT, so was the expression of P53 by immunohistochemical method. LDH activity in the extracellular fluid was determined and levels of SOD, MDA in the cell homogenate fluid were examined. Results As compared with those in the model group, the neuronal injury was markedly declined in the ASPS group and the neuronal activity was higher (0.46 vs 0.36, P < 0.01). The level of P53 expression was lower in the ASPS group and higher in the model group. The activities of LDH and the MDA level were evidently lower in the ASPS group than in the model group but the SOD activity was significantly higher. Conclusion ASPS can increase the capability of the hippocampal neuron to resist oxidation in a concentration-dependent manner.