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作 者:金勇君[1] 杨美子[2] 张凌云[1] 李建周[1] 刘欣[1]
机构地区:[1]滨州医学院附属医院内分泌科,山东滨州256603 [2]滨州医学院药理学教研室,山东烟台264003
出 处:《中国临床药理学杂志》2011年第10期767-769,共3页The Chinese Journal of Clinical Pharmacology
基 金:国家自然科学基金资助项目(30660070);山东省中青年科学家科研奖励基金资助项目(BS2010YY002)
摘 要:目的观察腺苷酸活化蛋白激酶(AMPK)在促黑素(α-MSH)对骨骼肌细胞脂肪酸氧化影响中的作用。方法用α-MSH、环磷酸腺苷(cAMP)类似物Bt2cAMP8、-BrcAMP和cAMP拮抗剂,分别处理体外培养的原代骨骼肌细胞(PMC)和C2C12成肌细胞后,测定脂肪酸氧化及AMPK活性。用cAMP拮抗剂RpcAMP预处理C2C12成肌细胞;再用α-MSH处理后,测定脂肪酸氧化和AMPK活性。结果α-MSH和cAMP类似物在骨骼肌细胞及C2C12成肌细胞中,显著增加了脂肪酸氧化及AMPK活性;但这些作用被cAMP拮抗剂显著抑制。结论α-MSH可能与黑皮质素受体(MCR)结合,并通过cAMP信号通路增加AMPK活性,而AMPK可促进骨骼肌细胞的脂肪酸氧化。Objective To investigate the role of AMP-activated protein kinase(AMPK) on fatty acid oxidation in skeletal muscle.Methods Primary muscle cells(PMC) and C2C12 cells were treated with α-melanocyte stimulating hormone(α-MSH),cyclic AMP(cAMP) analogs Bt2cAMP,8-BrcAMP and cAMP antagonist,respectively.C2C12 cells were pretreated with RpcAMP,cAMP antagonist,then α-MSH was added to the culture medium,and the AMPK activity and fatty aicd oxidation were measured.Results AMPK activity and fatty acid oxidation were significantly increased after treated with α-MSH and cAMP analogs,and the effects were significantly reduced after pretreated with cAMP antagonist in C2C12 cells.Conclusion α-MSH might be binding with melanocortin receptor(MCR) and through cAMP signal pathway enhances AMPK activity then increase fatty acid oxidation in skeletal muscle.
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