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目的研究褐藻多糖硫酸酯对H2O2诱导小鼠皮层神经元氧化损伤的保护作用,并探讨其作用机制。方法以含有B-27的Neurobasal培养基无血清体外原代培养新生小鼠大脑皮层神经元,H2O2(50μmol/L)诱导氧化应激损伤模型,MTT法检测不同质量浓度(0.01、0.1、1 g/L)褐藻多糖硫酸酯对细胞存活的影响,生化法测定乳酸脱氢酶(LDH)释放量和丙二醛(MDA)、超氧化物歧化酶(SOD)的活性。结果与H2O2处理组比较,0.1、1 g/L褐藻多糖硫酸酯能显著提高H2O2诱导损伤皮层神经元的存活率(P<0.05),并且降低培养液中LDH的漏出量,抑制细胞内MDA的生成,提高细胞内SOD的活性。结论褐藻多糖硫酸酯对H2O2损伤皮层神经元具有显著的保护作用,其机制与抗氧化作用有关。
Objective To study the protective effect of fucoidan on oxidative damage induced by H2O2 in mouse cortical neurons and to explore its mechanism. Methods Neurobasal medium containing B-27 was used to culture neonatal mouse cortical neurons in primary culture in vitro. H2O2 (50μmol / L) was used to induce oxidative stress injury. MTT assay was used to detect the effects of different concentrations (0.01,0.1,1 g / L) effects of fucoidan on cell viability. The release of lactate dehydrogenase (LDH) and the activities of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured by biochemical methods. Results Compared with H2O2 treatment group, 0.1,1 g / L fucoidan significantly increased the H2O2-induced survival of cortical neurons (P <0.05), decreased the amount of LDH leakage in the culture medium and inhibited the intracellular MDA Generate, improve intracellular SOD activity. Conclusions Fucoidan has a significant protective effect on cortical neurons injured by H2O2, the mechanism of which is related to antioxidation.