甘草苷对过氧化氢所致SH-EP1细胞株氧化应激损伤的保护作用研究

Protective effect of liquiritin on the oxidative stress injury of SH-EP1 cell lines caused by hydrogen peroxide

目的:研究甘草苷对过氧化氢所致SH-EP1细胞株氧化应激损伤的保护作用。方法:培养SHEP1细胞株并随机分为对照组、过氧化氢(H_2O_2)组以及甘草苷组,分别给予不含血清的培养基、200μmol/L的H_2O_2以及100、200、400μmol/L甘草苷联合200μmol/L的H_2O_2处理。处理后测定细胞活力值以及细胞中线粒体凋亡分子、抗氧化分子的含量。结果:处理12、24、36、48后,H_2O_2组的细胞活力值均显著低于对照组(P<0.05),100、200、400μmol/L甘草苷组的细胞活力值均显著高于H_2O_2组,且甘草苷剂量越大、细胞活力值越高(P<0.05);处理24 h后,H_2O_2组中Bax、Caspase-3、Nrf2、ARE的含量显著高于对照组(P<0.05),Bcl-2、凋亡抑制蛋白(XIAP)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GHS-Px)、血红素氧合酶(HO-1)的含量显著低于对照组(P<0.05);100、200、400μmol/L甘草苷组中Bax、Caspase-3的含量显著低于H_2O_2组(P<0.05),Bcl-2、XIAP、Nrf2、ARE、SOD、GHS-Px、HO-1的含量显著高于H_2O_2组且甘草苷剂量越大,Bax、Caspase-3的含量越低(P<0.05),Bcl-2、XIAP、Nrf2、ARE、SOD、GHS-Px、HO-1的含量越高(P<0.05)。结论:甘草苷能够通过抑制线粒体途径凋亡、增强抗氧化系统功能的途径来减轻过氧化氢所致SH-EP1细胞株氧化应激损伤。

Objective： To study the protective effect of liquiritin on the oxidative stress injury of SH-EP1 cell lines caused by hydrogen peroxide. Methods： SH-EP1 cell lines were cultured and randomly divided into control group,H2O2 group and liquiritin group that were treated with the culture medium without serum,200 μmol / L H2O2 as well as 100 μmol / L,200 μmol / L and 400μmol /L liquiritin combined with 200 μmol /L H2O2 respectively. After treatment,cell viability values as well as the content of mitochondrial apoptosis molecules and antioxidant molecules in cells were determined. Results： After 12 h,24 h,36 h and 48 h of treatment,the cell viability values of H2O2 group were significantly lower than those of control group,the cell viability values of 100 μmol /L,200 μmol / L and 400 μmol / L liquiritin group were significantly higher than those of H2O2 group and the larger the liquiritin dosage,the higher the cell viability value; after 24 h of treatment,Bax,Caspase-3,Nrf2 and ARE content of H2O2 group were significantly higher than those of control group while Bcl-2,XIAP,SOD,GHS-Px and HO-1 content were significantly lower than those of control group; Bax and Caspase-3 content of 100 μmol / L,200 μmol / L and 400 μmol / L liquiritin group were significantly lower than those of H2O2 group while Bcl-2,XIAP,Nrf2,ARE,SOD,GHS-Px and HO-1 content were significantly higher than those of H2O2 group,and the larger the liquiritin dosage,the lower the Bax and Caspase-3 content while the higher the Bcl-2,XIAP,Nrf2,ARE,SOD,GHSPx and HO-1 content. Conclusions： Liquiritin can inhibit the mitochondrial apoptosis and enhance the antioxidant system function to relieve the oxidative stress injury of SH-EP1 cell lines caused by hydrogen peroxide.