【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 protein 1,VDAC1）、线粒体裂变相关蛋白1（dynamin-related protein 1,DRP1）、线粒体融合蛋白2（mitofusin 2,MFN2）及AMP活化蛋白激酶（AMP-activated protein kinase, AMPK）表达；通过MitoTracker^TM Red CMXROs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。更多还原

【Abstract】 Objective To explore the protective effect and possible mechanism of Irisin on high glucose-induced renal proximal tubule cells injury.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 expression levels of KIM-1,VDAC1,DRP1,MFN2 and AMP activated protein kinase（AMPK）were detected by Western blotting; MitoTracker^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-DRP1⁶¹⁶in renal proximal tubule cells decreased, the expression of VDAC1,MFN2 and p-AMPK increased（all P<0.05）,the division rate of mitochondria in cells decreased significantly, and the structure of short rod-like or granular mitochondria decreased.Conclusion Irisin has a protective effect on high glucose-induced renal proximal tubule cells injury, and its mechanism may be related to the activation of AMPK,the maintenance of mitochondrial fission fusion balance, and the improvement of mitochondrial function.更多还原