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作 者:赵霞[1] 董津男[1] 林良妍[1] 张冬冬[1] 綦才辉[1] 金勇君[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
出 处:《中国临床药理学杂志》2013年第5期364-366,共3页The Chinese Journal of Clinical Pharmacology
基 金:国家自然科学基金资助项目(30660070);山东省优秀中青年科学家科研奖励基金资助项目(BS2010YY002)
摘 要:目的观察α-促黑素(α-MSH)促进脂肪酸氧化中的信号传导通路。方法 C2C12成肌细胞分成4组:对照组、α-MSH组、H-89加α-MSH组和RpcAMP加α-MSH组,分别处理后测定脂肪酸氧化和腺苷酸活化蛋白激酶(AMPK)活性。用免疫印迹法分组观察磷酸化的乙酰辅酶A羧化酶(ACC)。结果α-MSH组与对照组相比较显著增加了脂肪酸氧化和AMPK活性;但cAMP抑制剂(RpcAMP)和蛋白激酶A(PKA)抑制剂(H-89)均阻断了α-MSH的上述作用。免疫印迹法显示,α-MSH增加ACC的磷酸化,但同样被上述抑制剂阻断。结论α-MSH主要通过cAMP-PKA-AMPK-ACC的途径增加脂肪酸氧化。Objective To investigate the signal transduetion pathway on fatty acid oxidation by α- melanocyte stimulating hormone ( α- MSH). Methods The C2C12 cells were divided into 4 groups:control group, α- MSH group , H - 89 plus α- MSH group and RpcAMP plus α- MSH group. The fatty acid oxidation and AMP- activated protein kinase (AMPK) activity were measured through the above treated groups. The phosphorylation of acetyl CoA earboxylase (ACC)was observated by immunity signature law grouping. Results The fatty acid oxidation and AMPK activity were significantly increased in α-MSH compared with control group, but cyclic adenosine monophosphate (cAMP) inhibitor (RpcAMP) and protein kinase A (PKA) inhibitor ( H - 89) blocked the above action of α-MSH. The immunity siganature law demonstrated that α- MSH increased the phosphorylation of ACC, but it was blocked by the above inhibitors. Conclusion α- MSH mainly increased the fatty acid oxidation by cAMP - PKA - AMPK - ACC.
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