摘要
目的 验证PRKAR1A和SOS2是否为鼠李素改善多组织胰岛素抵抗的关键分子靶点,明确鼠李素对胰岛素抵抗细胞的调控作用。方法 以LHCN-M2人类骨骼肌细胞和人SGBS前脂肪细胞为研究对象,构建棕榈酸诱导的胰岛素抵抗细胞模型,采用鼠李素干预后,通过葡萄糖摄取实验检测细胞糖代谢能力,qPCR技术检测PRKAR1A和SOS2基因表达水平,蛋白质印迹法检测相关蛋白表达量。结果 胰岛素抵抗细胞经鼠李素干预后,葡萄糖摄取能力显著提升;PRKAR1A基因及蛋白表达水平显著降低,SOS2基因及蛋白表达水平显著升高;且鼠李素联合胰岛素的干预效果优于单独使用胰岛素(P<0.05)。结论 鼠李素可通过下调PRKAR1A、上调SOS2表达改善骨骼肌和脂肪细胞的胰岛素抵抗,PRKAR1A和SOS2是其关键作用靶点。
Objective To verify whether PRKAR1A and SOS2 are the key molecular targets through which rhamnetin ameliorates multi-tissue insulin resistance,and to clarify the regulatory effects of rhamnetin on insulin-resistant cells.Methods Human LHCN-M2 skeletal muscle cells and SGBS preadipocytes were selected as the research subjects to establish a palmitic acid-induced insulin resistance cell model.After intervention with rhamnetin,cellular glucose metabolic capacity was assessed via glucose uptake assays.The mRNA expression levels of PRKAR1A and SOS2 were measured via quantitative real-time polymerase chain reaction(qPCR),and the relative protein expression levels were determined by Western blotting.Results After rhamnetin intervention,the glucose uptake capacity of insulin-resistant cells was significantly enhanced.Furthermore,the mRNA and protein expression levels of PRKAR1A were markedly decreased,while those of SOS2 were significantly increased.Moreover,the therapeutic effect of rhamnetin combined with insulin was superior to that of insulin alone(P<0.05).Conclusion Rhamnetin can ameliorate insulin resistance in skeletal muscle cells and adipocytes by downregulating PRKAR1A expression and upregulating SOS2 expression,indicating that PRKAR1A and SOS2 are its key therapeutic targets.
作者
朱慧玲
吕菁
许立
ZHU Huiling;LV Jing;XU Li(School of Medicine,Wuhan University of Science and Technology,Wuhan Hubei 430000,China)
出处
《湖北科技学院学报(医学版)》
2026年第2期105-108,共4页
Journal of Hubei University of Science and Technology(Medical Sciences)
