鸢尾素通过激活AMPK抑制高糖诱导的肾小管上皮细胞线粒体损伤  

Irisin Inhibits High Glucose-induced Mitochondrial Damage in Kidney Proximal Tubule Epithelial Cells by Activating AMPK

作　　者：赵艺璇 彭薇 田蓓晨 柯琳 蔡阳 韩敏[1] 邓元俊 Zhao Yixuan;Peng Wei;Tian Beichen(Department of Nephrology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)

机构地区：[1]华中科技大学同济医学院附属同济医院肾内科,武汉430030

出　　处：《华中科技大学学报（医学版）》2023年第3期340-344,共5页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

摘　　要：目的探究鸢尾素(Irisin)对高糖诱导的肾小管上皮细胞损伤的保护作用及可能机制。方法体外培养近端肾小管上皮细胞(renal proximal tubule cells,TKPTs),细胞分为正常对照(NG)组、高渗对照(MA)组、高糖(HG)组、高糖+鸢尾素(HG+Irisin)组。利用蛋白印迹法测定肾损伤分子1(kidney injury molecular1,KIM-1)、电压依赖性阴离子通道1(recombinant voltage dependent anion channel protein1,VDAC1)、线粒体裂变相关蛋白1(dynamin-related protein 1,DRP1)、线粒体融合蛋白2(mitofusin2,MFN2)及AMP活化蛋白激酶(AMP-activatedproteinkinase,AMPK)表达;通过MitoTracker^(TM) RedCMXROs染色观察细胞内线粒体的形态。结果与NG组相比,HG组KIM1、p-DRP1616表达增加,VDAC1、MFN2、p-AMPK表达减少(均P<0.05);其细胞内线粒体分裂增加,线粒体呈短棒状或颗粒状。与HG组相比,加入Irisin干预后,近端肾小管上皮细胞KIM1、p-DRP1616表达减少,VDAC1、MFN2、p-AMPK表达增加(均P<0.05),细胞内线粒体的分裂明显减少,短棒状或颗粒状线粒体结构减少。结论Irisin对高糖诱导的近端肾小管上皮细胞损伤具有保护作用,其机制可能与激活AMPK,维持线粒体裂变-融合平衡,改善线粒体功能有关。Objective To explore the protective effect and possible mechanism of Irisin on high glucose-induced renal proxi-mal tubule cells inj ury.Methods Renal proximal tubule cells were cultured in vitro.The cells were divided into normal control group(NG),hypertonic control group(MA),high glucose group(HG),and high glucose+Irisin group(HG+Irisin).The ex-pression levels of KIM-1,VDAC1,DRP1,MFN2 and AMP activated protein kinase(AMPK)were detected by W estern blotting;MitoT racker^(TM) Red CMXROs staining was used to observe the morphology of mitochondria in cells.Results Compared with NG group,the expressions of KIM1 and p-DRP1616 increased,and the expressions of VDAC1,MFN2 and p-AMPK decreased in HG group(all P<0.05).The mitotic rate of mitochondria in the cells increased,and the mitochondria were short rod-like or granular.Compared with the HG group,after irisin intervention,the expression of KIM1 and p-DRP1616 in renal proximal tubule cells decreased,the expression of VDAC1,MFN2 and p-AMPK increased(all P<0.05),the division rate of mitochondria i cells decreased significantly,and the structure of short rod-like or granular mitochondria decreased.Conclusion Irisin has a pro-tective effect on high glucose-induced renal proximal tubule cells injury,and its mechanism may be related to the activation 0 AMPK,the maintenance of mitochondrial fission fusion balance,and the improvement of mitochondrial function.

关 键 词：近端肾小管上皮细胞 鸢尾素 AMP活化蛋白激酶 线粒体裂变-融合 

分 类 号：R692.6[医药卫生—泌尿科学]