摘要
目的通过敲减细胞内成纤维细胞生长因子21(fibroblast growth factors 21,FGF21)的表达,观察其对肝细胞脂质代谢的影响,并探讨FGF21调控肝细胞脂质代谢的分子机制。方法通过FGF21干扰慢病毒转染HepG2细胞,降低FGF21的表达,以空载体转染HepG2细胞作为对照,分为干扰组和对照组。两组均以棕榈酸油酸刺激构建非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)细胞模型。采用油红O染色法观察肝细胞内脂质沉积情况,测定分光光度值,计算脂质含量;利用蛋白质印迹(Western blot)法检测肝细胞中SOCS3、JAK2、STAT3蛋白的变化。结果油红O染色及吸光度值显示,与对照组相比,干扰组肝细胞内脂滴含量显著减少;Western blot结果表明,干扰组肝细胞内细胞因子信号转导抑制因子3(suppressor of cytokine signaling 3,SOCS3)、Janus激酶2(Janus kinase 2,JAK2)、信号转导和转录活化因子3(signal transducer and activator of transcription,STAT3)蛋白表达水平均显著升高。结论在肝细胞模型中,敲减FGF21表达,可通过激活SOCS3/JAK/STAT信号通路从而抑制肝细胞脂质沉积。但其具体作用机制仍需进一步深入研究。
Objective By knocking down the expression of fibroblast growth factors 21(FGF21)in adipose liver cells,to observe lipid metabolism and to explore the molecular mechanism of FGF21 regulating lipid metabolism in liver cells.Methods By interfering with lentivirus transfection through FGF21,the expression of FGF21 was reduced in HepG2 cells.HepG2 cells were transfected with an empty vector as a control,and were respectively referred to as interference group and control group.Both groups were stimulated with palmitic acid oleic acid to construct non-alcoholic fatty liver disease(NAFLD)cell model.The expression of FGF21 was interfered by lentivirus vector,oil red O staining and spectrophotometric value were measured to observe the lipid deposition in cells.Use Western blot method to detect the changes of suppressor of cytokine signaling 3(SOCS3),JAK2,and STAT3 proteins in fatty liver cells.Results Oil red O staining and absorbance values showed that compared with control group,interference group significantly reduced the lipid droplet content in liver cells;Western blot results showed that the expression levels of suppressor of cytokine signaling 3(SOCS3),Janus kinase 2(JAK2),signal transducer and activator of transcription 3(STAT3),and STAT3 protein were significantly increased in interference group of liver cells.Conclusion In the fatty liver cell model,knocking down FGF21 can improve lipid deposition through liver cells.The mechanism may be through increasing the SOCS3/JAK/STAT pathway,but the specific mechanism of action needs further in-depth research in the future.
作者
沈方方
祝峰
徐珂
滕懿群
SHEN Fangfang;ZHU Feng;XU Ke;TENG Yiqun(Department of Pediatrics,the Second Hospital of Jiaxing,Jiaxing 314501,Zhejiang,China)
出处
《中国现代医生》
2024年第9期12-16,共5页
China Modern Doctor
基金
嘉兴市科技计划项目(2021AD30125,2021AY30014)。
