褪黑素对亚油酸导致的胰岛素信号转导缺陷的修复机制

发布时间：2018-04-16 06:49

本文选题：胰岛素抵抗 + 活性氧自由基　；参考：《中国临床药理学杂志》2015年20期

【摘要】：目的探讨褪黑素(MT)对亚油酸(LA)引起Hep G2细胞胰岛素信号缺陷的修复作用及其机制。方法将培养的Hep G2细胞分为对照组(BSA组)、亚油酸组(LA组)、亚油酸+褪黑素组(LA+MT组)、亚油酸+维生素C组(LA+Vit C组)。BSA组予以10%牛血清白蛋白处理24 h;LA组予以0.5 mmol·L-1亚油酸处理24 h,LA+MT组予以10μmol·L-1褪黑素和0.5 mmol·L-1亚油酸处理24 h;LA+Vit C组予以1 mmol·L-1维生素C和0.5 mmol·L-1亚油酸处理24 h。用荧光比色法测定各组细胞胞内氧自由基水平,用Western印迹法检测胰岛素刺激后胞内胰岛素信号蛋白磷酸化水平,包括蛋白激酶B、叉头转录因子以及c-Jun氨基末端激酶。结果 LA组的氧自由基含量明显高于BSA组(P0.05);LA+MT组的氧自由基含量明显低于LA组(P0.05);LA+MT组与BSA组相比,氧自由基含量差异无统计学意义(P0.05)。LA+Vit C组与LA组相比,氧自由基的含量减少,但仍高于LA+MT组,差异有统计学意义(P0.05)。LA组与BSA组相比,蛋白激酶B、叉头转录因子磷酸化水平减少,而c-Jun氨基末端激酶磷酸化水平升高;LA+MT组与LA组相比,蛋白激酶B、叉头转录因子磷酸化水平显著升高,c-Jun氨基末端激酶磷酸化水平明显降低,组间比较差异有统计学意义(P0.05)。结论亚油酸可导致细胞内氧自由基增加,褪黑素能够清除亚油酸产生的过量氧自由基,减少c-Jun氨基末端激酶的活化,修复胰岛素下游信号损伤。
[Abstract]:Objective to investigate the effect and mechanism of melatonin (MT) on insulin signal defect in Hep G2 cells induced by linoleic acid (LA).Methods the cultured Hep G2 cells were divided into three groups: control group, linoleic acid group, linoleic acid group, linoleic acid melatonin group, LA MT group, linoleic acid vitamin C group, LA Vit C group and BSA group treated with 10% bovine serum albumin for 24 hours.The LA MT group was treated with 10 渭 mol L-1 melatonin and 0.5 mmol L-1 linoleic acid for 24 h. The LA Vit C group was treated with 1 mmol L-1 vitamin C and 0.5 mmol L-1 linoleic acid for 24 h.The intracellular oxygen free radicals were measured by fluorescence colorimetry, and the phosphorylation of insulin signaling proteins, including protein kinase B, fork head transcription factor and c-Jun amino terminal kinase, were detected by Western blotting.Results the content of oxygen free radical in LA group was significantly higher than that in BSA group (P 0.05). The content of oxygen free radical in LA group was significantly lower than that in LA group and BSA group. There was no significant difference in oxygen free radical content between LA group and BSA group. Compared with LA group, the content of oxygen free radical in LA Vit C group was lower than that in LA group.But the level of phosphorylation of protein kinase B and fork head transcription factor in LA MT group was lower than that in BSA group, while the phosphorylation level of c-Jun amino terminal kinase in LA MT group was higher than that in LA MT group.The phosphorylation level of protein kinase B and fork head transcription factor increased significantly, and the phosphorylation level of c-Jun amino terminal kinase decreased significantly. The difference between the two groups was statistically significant (P 0.05).Conclusion linoleic acid can increase the intracellular oxygen free radicals. Melatonin can scavenge the excessive oxygen free radicals produced by linoleic acid, reduce the activation of c-Jun amino terminal kinases, and repair the downstream signal damage of insulin.
【作者单位】：河南科技大学医学院生物化学与分子生物学教研室;天津市东丽区中医院外科;
【基金】：河南科技大学创新能力培育基金资助项目(2012ZCX024)
【分类号】：R96

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