摘要
目的探讨Ghrelin对高脂环境下成肌细胞解偶联蛋白3(UCP3)活化及乙酰CoA羧化酶(ACC)磷酸化的影响,为深入研究2型糖尿病的防治提供理论依据。方法原代培养大鼠成肌细胞0.3mmol/L棕榈酸处理12h,同时分别加入10^-11、10^-9、10^-7mol/LGhrelin作用,用RT-PCR法检测UCP3的mRNA表达,用Westernblotting法检测UCP3和p-ACC蛋白的水平。结果与对照组相比,在高脂组中,UCP3mRNA表达明显下降(P=0.000),UCP3和p-ACC蛋白水平明显降低(P=0.000,P=0.003)。与高脂组对比,干预组随着给予Ghrelin的浓度逐渐增加,UCP3mRNA表达明显增加,UCP3和p-ACC蛋白水平明显升高并呈剂量反应关系,其中10^-7mol/LGhrelin组改变最为明显(UCP3mRNA:P=0.017,UCP3蛋白水平:P=0.000,p-ACC蛋白水平:P=0.007)。结论Ghrelin对高脂环境下成肌细胞UCP3活化及ACC磷酸化具有促进作用。
Objective To study the effect of Ghrelin on activation of UCP3 and phosphorylation of ACC under the high fat environment in rat myoblast, and to support the study on prevention of type 2 diabetes. Methods The rat myoblast were exposed to 0. 3 mmol/L palmitic acid for 12 h, at the same time, 10^-11 mol/L, 10^-9 mol/L, 10^-7 mol/L Ghrelin were added. The expression of UCP3 mRNA was determinedby RT-PCR. The protein levels of UCP3 and p-ACC were measured by western blotting. Results Com- pared with the control group, UCP3 mRNA and the protein levels of UCP3 and p-ACC were obviously de- creased in 0. 3 mmol/L PA group(UCP3 mRNA: P =0. 000,UCP3 protein levels: P =0. 000,p-ACC pro- tein levels : P = 0. 003 ). Compared with the 0. 3 mmol/L PA group, with the increasing concentration of Ghrelin, UCP3 mRNA and the protein levels of UCP3 and p-ACC were elevated. The effects of 10 ^-7 mol/L Ghrelin were significant( UCP3 mRNA : P = 0. 017, UCP3 protein levels : P = 0. 000, p-ACC protein levels : P = 0. 007). Conclusions Ghrelin could enhance activation of UCP3 and phosphorylation of ACC under high fat environment in rat myoblast.
出处
《中国医师杂志》
CAS
2012年第2期163-165,169,共4页
Journal of Chinese Physician
基金
辽宁省教育厅科研项目计划(L2010598)