L6细胞中稳定敲除AMPKα1对抗糖尿病药物发挥作用的影响OA
Effect of stable knockout of AMPKα1 on anti-diabetic medication function in L6 cells
肌肉细胞对于葡萄糖的消耗是关乎体内血糖水平高低的关键步骤.单磷酸腺苷活化蛋白激酶(adenosine 5'-monophosphate(AMP)-activated protein kinase,AMPK)作为糖尿病药物治疗的关键通路,可以在被磷酸化激活后促进肌肉细胞中的葡萄糖摄取.为了探讨AMPKα亚基在糖尿病治疗中的关键作用,在L6大鼠骨骼肌细胞中使用规律成簇的间隔短回文重复系统(CRISPR/Cas9)敲除AMPKα1蛋白,以探究L6细胞中AMPKα1亚基的缺失对于糖尿病药物的治疗影响.结果表明,与对照相比,当AMPKα缺失后,二甲双胍促进的AMPKα亚基的磷酸化完全消失,并且二甲双胍在正常细胞中促进葡萄糖摄取的作用在敲除细胞中呈现降低趋势.研究揭示了 AMPKα1亚基在糖尿病药物作用中的关键地位,为精准靶向药物治疗及药物机制探究提供了重要实验模型.
The consumption of glucose by muscle cells is a key step in determining the level of blood sugar in the body.Adenosine 5'-monophosphate-activated protein kinase(AMPK),a key pathway in diabetes adenosine monophosphate,promotes glucose uptake in muscle cells when activated by phosphorylation.In order to explore the key role of AMPKαsubunit in the treatment of diabetes,AMPKα1 protein in L6 rat skeletal muscle cells was knocked out by using regularly clustered interspaced short palindromic repeats(CRISPR/Cas9)to explore the effect of AMPKα1 subunit deletion in L6 cells on the treatment of diabetes.The results showed that the metformin-promoted phosphorylation of AMPKα subunit completely disappeared when AMPKα was deleted,and the effect of metformin on glucose uptake in normal cells showed a decreasing trend in knockout cells.It reveals the key position of AMPKα1 subunit in the action of diabetic drugs,and provides an important experimental model for precise targeted drug therapy and drug mechanism exploration.
赵平;田贵林;杨新洲
中南民族大学 生命科学学院,湖北武汉 430074中南民族大学 生命科学学院,湖北武汉 430074中南民族大学 药学院,湖北武汉 430074
生物科学
单磷酸腺苷活化蛋白激酶葡萄糖摄取规律成簇的间隔短回文重复系统(CRISPR/Cas9)单磷酸腺苷活化蛋白激酶α1亚基
AMPKglucose uptakeCRISPR/Cas9AMPKα1
《中南民族大学学报(自然科学版)》 2026 (4)
483-488,6
国家自然科学基金资助项目(82474138)湖北省自然科学基金资助项目(2023AFC011)中央高校基本科研业务费专项资金资助项目(CZY23021)
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