Effects of Salvianolic Acid B on Mitochondrial Dysfunction and Fibrous Phenotype Transformation in HK-2 Cells Induced by High Glucose
- VernacularTitle:丹酚酸B对高糖诱导的HK-2细胞线粒体功能障碍及纤维化表型转换的影响
- Author:
Zhengwei DONG
1
;
Kang YANG
;
Xiaohong GUO
;
Huan ZHAO
Author Information
- Publication Type:Journal Article
- Keywords: Salvianolic acid B; HK-2 cells; Mitochondrial dysfunction; Phenotypic transformation of fibrosis
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2024;26(12):3145-3152
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the effect of Salvianolic acid B(SalB)on mitochondrial function and fibrosis phenotype of human renal proximal tubule cells(HK-2)induced by high glucose.Methods The dose of SalB in HK-2 was evaluated by CCK8 detection,and the effects of SalB on mitochondrial dysfunction and phenotypic transformation of cell fibrosis induced by high glucose were explored by qRT-PCR,Western blot and mitochondrial fluorescence probe.Results Compared with the control group,the number of mitochondria in HK-2 cells induced by high glucose decreased significantly(P<0.01),and high dose of SalB could significantly reduce the number of mitochondria.Compared with the control group,the expression level of CV-ATP5A protein in HK-2 cells induced by high glucose was significantly inhibited(P<0.01),and the expression of CV-ATP5A was significantly increased by low and high doses of SalB(P<0.01).Compared with the control group,the transcription levels of FN1,Coll3 and α-SMA in HK-2 cells induced by high glucose were significantly increased(P<0.05),and the intervention of SalB could significantly reduce the transcription levels of FN1,Coll3,MMP9 and α-SMA.Compared with the control group,the levels of FN1,Coll3 and α-SMA protein in HK-2 cells induced by high glucose were significantly increased,and the expression levels of FN1 and Coll3 protein could be significantly decreased by the intervention of SalB.Conclusion SalB,the main active component of Salvia miltiorrhiza,can improve the mitochondrial dysfunction of HK-2 cells induced by high glucose and effectively inhibit the phenotypic transformation of fibrosis.
