草苁蓉多糖对HepG2细胞氧化应激的抑制作用

Inhibitory Effect of Polysaccharides from Boschniakia Rossica on Oxidative Stress in HepG2 Cells

研究草苁蓉多糖(BRPS)对过氧化氢(H_2O_2)所致HepG2细胞氧化应激的抑制作用。以HepG2细胞为研究对象,通过H_2O_2诱导细胞氧化应激损伤模型,采用四甲基偶氮唑盐比色(MTT)法检测细胞存活率;比色法检测培养液中乳酸脱氢酶(LDH)、谷草转氨酶(AST)、谷丙转氨酶(ALT)活性以及细胞中超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)及丙二醛(MDA)水平;蛋白印迹法测定细胞外信号调节蛋白激酶(ERK)、c-Jun氨基末端激酶(JNK)、p38丝裂原活化蛋白激酶(p38)活化水平。结果表明,BRPS在质量浓度12.5 mg/L^50 mg/L范围内对HepG2细胞存活率无显著影响,对细胞安全。而H_2O_2诱导使HepG2细胞存活率和抗氧化能力下降,细胞内ERK和JNK磷酸化水平升高。与H_2O_2模型组相比,BRPS预处理可提高细胞存活率;降低培养液中LDH、AST和ALT活性;降低细胞内MDA含量,升高细胞中SOD活性和GSH含量,降低细胞内ERK和JNK磷酸化水平。提示,BRPS对H_2O_2所致HepG2细胞氧化应激具有抑制作用,减轻其细胞损伤。

Inhibitory effect of polysaccharides from Boschniakia rossica （BRPS） on cellular oxidative stress in- duced by hydrogen peroxide （H202） in HepG2 cell line was investigated. The cellular oxidative stress model was established in HepG2 cells with H202, and then the cell viabilities were detected with MTF assay. Lactate dehy- drogenase （LDH）, alanine aminotransferase （ALT）, aspartate aminotransferase （AST）, malondialdelyde （MDA）, superoxide dismutase （SOD） and reduced glutathione （GSH） were measured by the spectrophoto- metric method. The activation of extracellular signal-regulated kinase （ERK）, c-Jun N-terminal kinase （JNK）, p38 mitogen-activated protein kinase （p38） were determined with the western blotting method. Results showed that BRPS had no toxic effect on cultured HepG2 cells at the concentrations of 12.5 mg/L-50 mg/L. However, H202 decreased the cell viability and antioxidant activities, and increased activation of ERK and JNK. In HepG2 cells with HzO2-indueed oxidative stress, the administration of BRPS increased the cell viabili- ty, reduced LDH, ALT and AST leakage, reduced the MDA formation, increased the SOD and GSH levels, and suppressed the activation of ERK and JNK. Taken together, BRPS had the inhibitory effect on oxidative stress induced by H20z in HepG2 cells, and could relieve the oxidative damage of HepG2 cells