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作 者:刘欣[1] 金勇君[1] 杨美子[2] 张凌云[1] 乔珍[1]
机构地区:[1]滨州医学院烟台附属医院内分泌科,山东烟台264100 [2]滨州医学院药理学教研室,山东烟台264003
出 处:《中国现代医学杂志》2012年第17期12-16,共5页China Journal of Modern Medicine
基 金:国家自然科学基金(No:30660070);山东省中青年科学家科研奖励基金(No:BS2010YY002)
摘 要:目的观察黑皮质素受体(MCR)种类在促黑素(α-MSH)对小鼠骨骼肌细胞脂肪酸氧化影响中的作用。方法α-MSH、(Glu6)α-MSH、SHU9119、α-MSH+SHU9119处理体外培养的原代骨骼肌细胞和C2C12成肌细胞后测定脂肪酸氧化。siRNA方法抑制C2C12成肌细胞MC5R后观察α-MSH、SHU9119对脂肪酸氧化的影响。结果α-MSH在骨骼肌细胞及C2C12成肌细胞中剂量依赖性地增加了脂肪酸氧化,SHU9119和α-MSH+SHU9119处理组也显著增加了脂肪酸氧化,但(Glu6)α-MSH处理组对脂肪酸氧化无统计学意义。siRNA方法抑制MC5R,显著降低了α-MSH和SHU9119促进脂肪酸氧化的作用。结论α-MSH通过MC5R促进骨骼肌细胞脂肪酸氧化。【Objective】 To investigate the role of melanocortin receptor(MCR) subtype in the effect of α-Melanocyte stimulating hormone(α-MSH) on fatty acid oxidation in skeletal muscle.【Methods】 Muscle and C2C12 cells were treated with α-MSH, α-MSH,SHU9119 and α-MSH+ SHU9119,respectively,and the fatty acid oxidation was measured.C2C12 cells were transfected with siRNA designed to suppress MC5R expression,and treated with α-MSH and SHU9119,respectively,and the fatty acid oxidation was measured.【Results】 α-MSH dose-dependently increased the fatty acid oxidation in the C2C12 cells and primary culture skeletal muscle cells.Fatty acid oxidation was significantly increased after treated with SHU9119 and α-MSH+SHU9119,and siRNA against MC5R suppressed this effect.【Conclusion】 α-MSH through MC5R increased fatty acid oxidation in skeletal muscle.
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