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目的研究硒对氧化损伤大鼠肝细胞糖代谢关键酶表达的影响,并初步探讨其作用机制。方法采用0.1 mmol/L的H2O2建立氧化损伤细胞模型,并施加不同剂量硒干预,通过实时定量PCR技术检测葡萄糖激酶(glu-cok inse,GK)、糖原合成酶(glycogen synthase,GS)和蛋白激酶B(protein kinase B,PKB/Akt)的mRNA表达,并采用蛋白免疫印迹(W estern-b lot)方法检测Akt的蛋白表达水平。结果补硒各组GK的mRNA表达量为(9.692~16.588)×10-6,均高于H2O2损伤组(P<0.05);高剂量补硒组GS和Akt的mRNA表达量分别为57.618×10-6和0.2398×10-3,均高于H2O2损伤组(P<0.05);补硒各组Akt的蛋白表达量为(0.3343~0.4346)×10-3,均高于H2O2损伤组(P<0.05)。结论补硒可以在一定程度上改善氧化损伤对肝细胞糖代谢关键酶GK、GS的影响,其机制可能与上调胰岛素信号传导通路的关键信号分子Akt的表达有关。
Objective To study the effect of selenium on expression of key enzymes of hepatic glucose metabolism in rats with oxidative damage and to explore its mechanism. Methods Oxidative injury cell model was established by using 0.1 mmol / L H2O2 and different concentrations of selenium were used to detect the expression of glucokinase (GK), glycogen synthase (GS) and protein The protein expression of PKB / Akt was detected by Western blotting. The protein expression of Akt was detected by Western blotting. Results The mRNA expression of GK in selenium-supplemented groups was (9.692-16.588) × 10-6, higher than that in H2O2-injured groups (P <0.05). The mRNA expression of GS and Akt in high-selenium group was 57.618 × 10 -6 and 0.2398 × 10-3, respectively, which were higher than those in H2O2-injured group (P <0.05). The protein expression of Akt in selenium-supplemented groups was (0.3343 ~ 0.4346) × 10-3, 0.05). Conclusion Selenium supplementation may improve the oxidative damage to GK, GS, a key enzyme of hepatic glucose metabolism. The mechanism may be related to up-regulating the expression of Akt, a key signaling molecule in insulin signaling pathway.