Mechanism of lipotoxicity-associated apoptosis mediated by mitochondrial dysfunction in pancreatic β-cells
- VernacularTitle:线粒体功能障碍在胰岛β细胞脂性凋亡中的作用
- Author:
Wei WANG
;
Dan ZHANG
;
Ying CHEN
;
Cuiping CAO
;
Lingling HAN
;
Guoliang LIU
- Publication Type:Journal Article
- Keywords:
Mitochondria;
MIN6 cells;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2010;26(1):163-166
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the mechanism of lipotoxicity-associated apoptosis mediated by mitochondrial pathway in pancreatic β-cells. METHODS:The pancreatic β-cell line MIN6 cells were incubated respectively in serum-free DMEM medium with or without palmitate (0.1-0.5 mmol/L) for 24 h,followed by Hoechst 33258 staining. The activity of caspase 3 was assayed for determining apoptosis,transmission electron microscope was used for observing mitochondrial structure,and RT-PCR analysis was applied for detection of mRNA expression of bcl-2-associated X protein (bax),B-cell lymphoma 2 (bcl-2),sterol regulatory element binding transcription factor 1c (SREBP1c) and DNA-damage inducible transcript 3 (chop-10). RESULTS:Palmitate induced apoptosis of MIN6 cells and swelling of mitochondria. Palmitate also inhibited mRNA expression of bcl-2,whereas enhanced mRNA expression of bax,SREBP1c and chop-10. CONCLUSION:Palmitate induces apoptosis of pancreatic β-cells by promoting mitochondrial dysfunction,which is associated with abnormal expressions of bax,bcl-2,SREBP1c and chop-10.
