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目的探讨抑制线粒体氧化磷酸化系统各复合物对细胞糖酵解的影响。方法培养HepG2细胞,铺于96孔板,用不同浓度的线粒体氧化磷酸化系统各复合物抑制剂处理24 h后,通过检测乳酸脱氢酶(LDH)释放量确定其最大无毒剂量;用小于该最大无毒剂量的各复合物抑制剂处理细胞后,通过检测培养基的葡萄糖和乳酸浓度,判断各复合物抑制剂对细胞糖酵解的影响。结果线粒体复合物Ⅰ、Ⅲ、Ⅴ抑制剂二甲双胍(metformin,Met)、黏噻唑(myxothiazol,Myxo)和寡霉素A(oligomycin A,Olig)可促进HepG2细胞葡萄糖消耗和乳酸生成,且其中二甲双胍的作用最强,黏噻唑其次,寡霉素A的作用最弱;线粒体复合物Ⅱ抑制剂2-噻吩甲酰三氟丙酮(2-thenoyltrifluoroacetone,TTFA)则可减少HepG2细胞葡萄糖消耗和乳酸生成;线粒体复合物Ⅳ抑制剂氰化钾(KCN)对HepG2细胞葡萄糖消耗和乳酸生成无影响。结论抑制线粒体复合物Ⅰ、Ⅲ、Ⅴ对细胞糖代谢是有益处的;抑制线粒体复合物Ⅳ对细胞糖代谢无作用;而抑制线粒体复合物Ⅱ阻碍了细胞的糖代谢。
Objective To investigate the effects of various compounds that inhibit mitochondrial oxidative phosphorylation system on cell glycolytic activity. Methods HepG2 cells were cultured in 96-well plates and treated with different concentrations of mitochondrial oxidative phosphorylation system for 24 h. The maximum non-toxic dose was determined by measuring the release of lactate dehydrogenase (LDH) After the maximum toxic dose of each complex inhibitor was treated, the effect of each complex inhibitor on the cell glycolytic activity was examined by measuring the glucose and lactate concentrations in the medium. Results Metformin (Met), myxothiazol (Myxo) and oligomycin A (Olig), inhibitors of mitochondrial complex Ⅰ, Ⅲ and Ⅴ, promoted glucose consumption and lactate production in HepG2 cells, and metformin In addition, the effect of oligothromycin A was the weakest. In addition, 2-thenoyltrifluoroacetone (TTFA), a mitochondrial complex Ⅱ inhibitor, reduced glucose consumption and lactate production in HepG2 cells. Mitochondria Compound Ⅳ inhibitor KCN had no effect on glucose consumption and lactate production in HepG2 cells. Conclusion Inhibition of mitochondrial complex Ⅰ, Ⅲ, Ⅴ is beneficial to the cellular glucose metabolism. Inhibition of mitochondrial complex Ⅳ has no effect on cellular glucose metabolism. Inhibition of mitochondrial complex Ⅱ hinders cellular glucose metabolism.