Cytoprotective mechanism of torularhodin against oxidative stress
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摘要: 探究红酵母红素对氧化应激细胞的保护机制。PC12细胞（大鼠肾上腺嗜铬细胞瘤细胞）分为对照组、模型组（200μmol/L H2O2）、番茄红素组（20μmol/L番茄红素+200μmol/L H2O2,阳性对照组）和红酵母红素组（1μmol/L红酵母红素+200μmol/L H2O2、2μmol/L红酵母红素+200μmol/L H2O2和3μmol/L红酵母红素+200μmol/L H2O2）,分别观察PC12细胞的形态变化,检测细胞凋亡率、半胱氨酸蛋白酶Caspase-3的活性及细胞中促凋亡蛋白Bax和抗凋亡蛋白Bcl-2的表达含量。结果表明,与模型组相比,3μmol/L的红酵母红素能维持细胞原有形态,降低了11.6%的细胞凋亡率（p<0.05）,抑制了62.92%的Caspase-3活性（p<0.01）,进一步研究发现红酵母红素能够下调Bax的表达（p<0.01）,上调Bcl-2的表达（p<0.01）,从而阻止了凋亡链反应。综上所述,红酵母红素可能通过抑制Caspase-3活性,调节Bax和Bcl-2的表达来发挥对氧化应激细胞的保护作用,且其作用存在剂量依赖性。Abstract: This study aims to investigate the cytoprotective mechanism of torularhodin against oxidative stress.PC12 cells were randomly divided into control group and model group( 200 μmol/L H2O2), lycopene group(20 μmol/L lycopene+200 μmol/L H2O2,positive control group) and torularhodin groups(1 μmol/L torularhodin+200 μmol/L H2O2,2 μmol/L torularhodin+200 μmol/L H2O2 and 3 μmol/L torularhodin+200 μmol/L H2O2). The changes of PC12 cell morphology were observed,while the apoptosis rate of cell,the activity of Caspase-3 and expressions of pro-apoptotic protein Bax and anti-apoptotic protein Bcl-2 were also detected. Results showed that 3 μmol/L torularhodin could maintain the original shape of cell,reduce 11.6% apoptosis rate(p<0.05) and inhibit 62.92% Caspase-3 activity(p<0.01),comparing with the model group. Further study demonstrated that torularhodin could down-regulate the expression of Bax(p<0.01) and up-regulate the expression of Bcl-2(p<0.01),which thereby prevented chain reaction of apoptosis and protected cells from oxidative stress. In a word,torularhodin could effectively protect cells against oxidative stress,by mechanisms which probably involves the inhibition of Caspase-3 activity and adjustment of Bax,Bcl-2 expression in dose-dependent manner.
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Keywords:
- torularhodin /
- oxidative stress /
- protect mechanism /
- PC12 cells /
- apoptosis
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