褪黑素通过抑制ROS改善胰岛素抵抗HepG2细胞糖代谢
Melatonin ameliorates glucose metabolism via inhibiting ROS generation ininsulin resistant HepG2 cells induced by high glucose and insulin
投稿时间:2014-06-09  修订日期:2014-06-09
DOI:
中文关键词:  褪黑素  胰岛素抵抗  葡萄糖摄取  糖原  ROS
英文关键词:MLT  insulin resistance  glucose uptake  glycogen  ROS
基金项目:国家教育部博士点基金;国家自然科学基金项目(面上项目,重点项目,重大项目)
作者单位E-mail
佘美华 南华大学药学与生物科学学院生物技术系 shemhbb@163.com 
蒋文艳 南华大学药学与生物科学学院生物技术系  
张瑶 南华大学药学与生物科学学院生物技术系  
杨娟 南华大学药学与生物科学学院生物技术系  
尹卫东 南华大学药学与生物科学学院生物技术系 shemhbb@163.com 
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中文摘要:
      目的 探讨褪黑素(melatonin, MLT)对胰岛素抵抗(insulin resistance, IR)HepG2细胞葡萄糖代谢的影响及机制。方法 培养HepG2细胞,高糖高胰岛素(25 mmol/L葡萄糖、1 μmol/L胰岛素)诱导24h,建立IR细胞模型并给予MLT(1 nmol/L, 10 nmol/L)处理。葡萄糖氧化酶法、蒽酮法和荧光探针法检测HepG2细胞的糖摄取、糖原含量及活性氧(reactive oxygen species, ROS)产率。结果 HGI孵育HepG2细胞24 h后,细胞的葡萄糖摄取及糖原含量明显减少(P < 0.01),ROS产率显著增加(P < 0.01);而MLT处理增加了IR细胞葡糖糖的摄取(P < 0.01)和糖原合成(P < 0.05),降低ROS的水平(P < 0.01)。结论 MLT可能通过抑制ROS的生成而改善氧化应激,从而促进胰岛素抵抗HepG2细胞葡萄糖的摄取和利用、增强其胰岛素敏感性。
英文摘要:
      Aim To investigate the effects of melatonin on glucose metabolism in high glucose and insulin-induced insulin resistant HepG2 cells. Methods Insulin resistant HepG2 cells were induced by high glucose and insulin (HGI, 25 mmol/L and 1 μmol/L respectively) coculture for 24 h, and then melatonin was added. The uptake of glucose was measured by glucose oxidase method, anthrone method was used to detect the Glycogen synthesis and fluorescence probe was used to detect ROS production. Results HGI incubating led to significant decreases in insulin-stimulated glucose uptake and glycogen synthesis in HepG2 cells (P < 0.01), but ROS production increased (P < 0.01). However, MLT treatment reversed the above state by increasing glucose uptake (P < 0.01) and glycogen synthesis (P < 0.05), inhibiting the generation of ROS(P < 0.01). Conclusions MLT could improve oxidative stress by inhibiting the production of ROS, and thereby increase glucose utilization and improve insulin sensitivity of insulin resistance HepG2 cells.
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