Cer(d18:1/16:0)Promotes Mitochondrial Dysfunction and Fibrotic Phenotype Transformation in HK-2 Cells
- VernacularTitle:Cer(d18:1/16:0)促进HK-2细胞线粒体障碍和纤维化表型转换
- Author:
Zhengwei DONG
1
;
Kang YANG
;
Xiaohong GUO
;
Huan ZHAO
Author Information
- Publication Type:Journal Article
- Keywords: Diabetic kidney disease; Cer(d18:1/16:0); HK-2 cells; Phenotypic transformation of fibrosis; Mitochondrial dysfunction
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2024;26(10):2545-2552
- CountryChina
- Language:Chinese
- Abstract: Objective To explore the effect of Cer(d18:1/16:0),the core marker in the development of diabetic kidney disease(DKD),on mitochondrial dysfunction and phenotypic transformation of human renal proximal tubule cells(HK-2)induced by high glucose.Methods With the help of qRT-PCR technology,the expression of ceramide synthesis related enzymes in HK-2 cells stimulated by high glucose was detected at the transcription level.The effects of different concentrations of Cer(d18:1/16:0)on the viability of HK-2 cells were detected by CCK8 method.The changes of mitochondrial number in HK-2 cells stimulated by different concentrations of Cer(d18:1/16:0)were evaluated by mitochondrial fluorescent probe.Western blot was used to detect the expression of mitochondrial related proteins and fibrosis indexes before and after the administration of Cer(d18:1/16:0).Results The expression of Ceramide synthase 2,(CERS2)in HK-2 cells increased in high glucose environment.Exogenous Cer(d18:1/16:0)can significantly inhibit the viability of HK-2 cells,can reduce the total and average fluorescence intensity of mitochondria in HK-2 cells induced by high glucose.The protein expression of CV-ATP5A and CIII-UQCRC2 decreased,while the protein expression of Coll 3,MMP9 and α-SMA increased.Conclusion Cer(d18:1/16:0)can induce mitochondrial dysfunction and fibrotic phenotype transformation in HK-2 cells stimulated by high glucose.
