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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 effect of quercetin derivative HPS5 on alcohol-induced oxidative damage in PC12 cells. Methods The model of PC12 cells was induced by alcohol. The inhibition rate of cells was detected by MTT assay. The activity of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase SOD and glutathione peroxidase (GSH), and Western-Blot were used to detect the expression of Bax and Bcl-2 protein. Results Compared with the model group, 25,50,100 mmol / L HPS5 could significantly reduce the inhibitory effect of alcohol on the proliferation of PC12 cells [(28.87 ± 2.34)%, (16.49 ± 2.13)%, (10.31 ± 1.17)%] LDH leakage [(36.47 ± 3.29), (31.67 ± 3.25), (29.34 ± 2.87) U / L] decreased MDA levels [1.89 ± 0.14], (1.61 ± 0.51), (1.48 ± 0.41) nmol / mg ], 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) (0.31 ± 0.03), (0.29 ± 0.03), (0.27 ± 0.03)], and increased the expression of Bcl-2 protein [(0.34 ± 0.01), (0.31 ± 0.02), (0.28 ± 0.02)] expression level. Especially in the high-dose group was more obvious, compared with the model group, the difference was statistically significant (P <0.05). Conclusions HPS5 can protect PC12 cells from alcohol injury, and it may be one of the mechanisms by which HPS5 can protect cells against oxidative stress and up-regulate the expression of Bcl-2 and down-regulate Bax protein.