二氢杨梅素对辐射引起神经元凋亡的保护作用

Protective Effects of Dihydromyricelin on Neuron Apoptosis Induced by Gamma-Radiation

目的探讨二氢杨梅素对γ射线辐射引起皮层神经元凋亡的保护作用和可能作用机制。方法原代培养的大鼠皮层神经元提前给予二氢杨梅素,1h后以8Gy辐射强度的γ射线照射10min。24h后MTT检测细胞存活率,试剂盒测试丙二醛和超氧阴离子的含量以及Caspase-9和Caspase-3的活性,Western blot检测细胞色素C、Bcl-2和Bax的表达。结果二氢杨梅素可剂量依赖性地提高γ射线辐射的细胞存活率,显著降低丙二醛和超氧阴离子的含量,抑制Caspase-9和Caspase-3的活性,抑制细胞色素C的释放以及Bcl2和Bax的比值,从而保护神经元。结论二氢杨梅素对γ射线引起的皮层神经元损伤有保护作用,这可能与其抑制氧化应激和细胞凋亡有密切关系。

Objective To investigate the protective effects of dihydromyricelin（DHM）on neuron apoptosis induced by gamma-radiation.Methods Primarily cultured cortical neurons were obtained from rats which were 19 dpregnant.The neurons were pre-incubated with DHM for 1 hbefore being subjected to gamma-radiation for 10 min at an intensity of 8 Gy.The biomarkers related to oxidative stress and apoptosis,such as the contents of malondialdehyde（MDA）and superoxide anion,the activities of Caspase-9 and Caspase-3,and the expression of cytochrome c（Cyt C）as well as Bcl-2,Bax,were measured.Results DHM dose-dependently increased cell viabilities of neurons exposed to gamma-radiation.DHM significantly reduced the production of MDA and superoxide anion.DHM markedly inhibited the activities of Caspase-9 and Caspase-3.Furthermore,the expression of CytC in the mitochondria and the ratio of Bcl-2 to Bax were increased by DHM treatment.Conclusion DHM has potent neuroprotective effects against gamma-radiation,which maybe closely related to the anti-oxidative stress and apoptosis of DHM.