›› 2009, Vol. 29 ›› Issue (8): 922-.

• Original article (Basic research) • Previous Articles     Next Articles

Pancreatic beta cell apoptosis inhibited by visfatin via mitochondrial pathways

CHENG Qun, PENG Yong-de, DONG Wei-ping, WANG Yi-fei, WU Jing-cheng, DING Xiao-ying   

  1. Department of Endocrinology and Metabolism, The First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China
  • Online:2009-08-25 Published:2009-09-27
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 74119638, 064119517

Abstract:

Objective To investigate the effects of visfatin on palmitate-induced islet β cell apoptosis.  Methods Mouse pancreatic cell line MIN6 was performed in vitro serial subcultivation, and subjected to experiment during exponential phase of growth. Cell viability of MIN6 was detected by MTT assay 24 to 72 h after induction by visfatin with different concentrations (0 to 10-7 mol/L). Cell apoptosis rate of MIN6 was examined by flow cytometry after induction by 0.5 mmol/L palmitate and/or 10-8 mol/L visfatin for 24 h, and expression of bcl-2, bax, cleaved caspase-3 and cytochrome C in endochylema was determined by Western blotting. Results Cell viability of MIN6 increased in a dose-dependent manner after treatment with visfatin for 24 to 48 h (P<0.05). It was revealed by flow cytometry that palmitate-induced apoptosis significantly reduced by 10-8 mol/L visfatin (P<0.05). It was demonstrated by Western blotting that 10-8 mol/L visfatin significantly inhibited the decreased expression of bcl2 and increased expression of cleaved caspase3 and cytochrome C induced by palmitate (P<0.05). Conclusion Visfatin may promote proliferation of pancreatic β cells, and inhibit palmitate-induced islet β cell apoptosis via mitochondrial pathways.

Key words: visfatin, palmitate, pancreatic &beta, cell, apoptosis

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