查尔酮类衍生物G01对H_2O_2诱导小鼠皮层神经元氧化损伤保护作用研究

Protective Effects of a Chalcone Derivative G01 on H_2O_2-induced Oxidative Damage in Cortical Neurons of Mice

本文研究查尔酮类衍生物G01(3'-甲酰基-4',6'-二羟基-2'-甲氧基-5'-甲基-3,4-二羟基查尔酮)对H_2O_2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。Neurobasal(含有B-27)的培养基无血清体外原代培养新生小鼠大脑皮层神经元,H_2O_2(50μmol/L)诱导氧化应激损伤模型,MTT法检测不同浓度(0.001、0.01、0.1 g/L)G01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)、超氧歧化酶(SOD)的含量。与H_2O_2处理组比较,0.01、0.1 g/L G01能显著提高H_2O_2诱导损伤皮层神经元的生存率74.51%,81.31%(P<0.05),并且降低了培养液中乳酸脱氢酶(LDH)的漏出量,抑制细胞内丙二醛(MDA)的生成,提高细胞内超氧歧化酶(SOD)的活性。研究结果表明G01对H_2O_2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。

This study was designed to investigate the protective effects of a new chalcone derivative G01,3＇-formyl-4＇, 6＇- dihydroxy-2＇-methoxy-5＇-methyl-3,4-dihydroxy chalcone, on H2 02 -induced oxidative damage in cortical neurons of mice, and the underlying mechanisms. Primary cortical neurons of newborn mice were cultured in Neurobasal containing B-27, free of serum, and the oxidative damage was induced by 50 p.mol/L H2 02. After the damage, the effects of different concentrations of G01 （0.001,0.01,0o 1 g/L） on cell survival was tested by MTr assay, and the levels of LDH, MDA and SOD were measured by biochemistry assay. Compared with the damage group,0.01,0.1 g/L C01 significantly improved the survival rate of neurons to 74.51% and 81.31% ,respectively,reduced the release of LDH in the medium, inhibited MDA synthesis, and enhanced the activity of SOD. These results indicated COl had significantly protective effects against H202-induced damage in cortical neurons,and the mechanisms were related to its antioxidative effects.