摘要
目的探讨槲皮素衍生物HPS5对酒精导致的PC12细胞氧化损伤的保护作用。方法酒精诱导PC12细胞建立模型,MTT法检测细胞的抑制率,比较治疗后乳酸脱氢酶(lactate dehydrogenase,LDH)活性,以及丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH)的水平,Western-Blot检测Bax和Bcl-2蛋白表达水平。结果与模型组比较,25、50、100 mmol/L HPS5能显著下调酒精对PC12细胞增殖的抑制作用[(28.87±2.34)%、(16.49±2.13)%、(10.31±1.17)%],减少LDH的漏出[(36.47±3.29)、(31.67±3.25)、(29.34±2.87)U/L],降低MDA水平[(1.89±0.14)、(1.61±0.51)、(1.48±0.41)nmol/mg],升高GSH[(81.25±8.33)、(92.14±9.34)、(96.24±11.24)mg/g]、SOD[(3.26±0.69)、(4.17±0.68)、(4.24±0.71)NU/mg]的水平,下调Bax蛋白[(0.31±0.03)、(0.29±0.03)、(0.27±0.03)]表达,升高Bcl-2蛋白[(0.34±0.01)、(0.31±0.02)、(0.28±0.02)]表达水平。尤其中高剂量组更加明显,与模型组比较,差异均有统计学意义(P<0.05)。结论 HPS5对酒精诱导的PC12细胞损伤具有保护作用,增强细胞的抗氧化能力以及上调Bcl-2和下调Bax蛋白的表达可能是其作用的机制之一。
Objective To investigate the protective effects of quercetin derivatives HPS5 against alcohol-induced oxidative damage in PC12 cells.Methods Alcohol was used to establish the oxidative damage model of PC12 cells.The viability of PC12 cells was determined by MTT assay.Lactate dehydrogenase(LDH) activity,the level of MDA,SOD and GSH were compared after treatment.The expression levels of Bax and Bcl-2 protein were detected by Western blotting.Results Compared with model group,HPS5 could significantly down-regulate the inhibition of PC12 cells by alcohol at the dose of 25,50 and 100 mmol/L [(28.87±2.34)%,(16.49±2.13)%,(10.31±1.17)%],and decrease significantly LDH release [(36.47±3.29),(31.67±3.25),(29.34±2.87) U/L] and MDA level[(1.89±0.14),(1.61±0.51),(1.48±0.41) nmol/mg],increase significantly GSH activity [(81.25±8.33),(92.14±9.34),(96.24±11.24) mg/g] and SOD activity [(3.26±0.69),(4.17±0.68),(4.24±0.71) NU/mg],down-regulate significantly Bax level[(0.31±0.03),(0.29±0.03),(0.27±0.03)]and increase significantly Bcl-2 level [(0.34±0.01),(0.31±0.02),(0.28±0.02)].It was particularly obvious in the high dose group.Compared with the model group,the difference was statistically significant(P0.05).Conclusion Quercetin derivatives HPS5 has protective effects against alcohol-induced oxidative damage in PC-12 cells.Enhancing the antioxidant capacity of cells,up-regulating Bcl-2 and down-regulating Bax protein may be one of the mechanisms.
出处
《社区医学杂志》
2014年第15期5-8,共4页
Journal Of Community Medicine