Exogenous H2S prevents high glucose-induced damage to osteoblasts through regulation of KATP channels

Publication date: Available online 18 March 2017
Source:Biochimie
Author(s): Yuanyuan Liu, Jianyong Liu, Xin Li, Fantao Wang, Xin Xu, Chunling Wang
Association between diabetes and osteoporosis has been extensively investigated. However, whether the effects of H2S on osteoblast function under high glucose (HG) condition relate to ATP-sensitive potassium (KATP) channels is unclear. To investigate the effects of H2S on the proliferation, apoptosis, and mineralization of osteoblasts under HG condition, and to observe whether H2S exert this effect through the KATP channels. Primary osteoblasts (POBs) were obtained from the calvaria of Sprague-Dawley rats. Cells were pre-treated with 400 μmol/L NaHS (a H2S donor), and/or 0.1 mmol/L non-selective KATP channel opener pinacidil (Pia), and/or KATP channel inhibitor glibenclamide (Gli). They then were cultured in DMEM with 26.5 mmol/L (HG) or 5.5 mmol/L (control) glucose. Cell proliferation, apoptosis, and mineralization were determined. In addition, expression of KATP SUR1 was also determined. NaHS pretreatment significantly inhibited the HG down-regulation of KATP SUR1 expression in POBs. NaHS also significantly prevented osteoblast injury induced by HG, through decreasing the rate of cell proliferation and increasing the number of apoptotic cells, which was similar with the effects of Pia. In addition, NaHS significantly deterred the HG-induced POB mineralization inhibition. H2S prevents the HG-induced osteoblast damage through regulation of KATP channels.



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