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

Association between diabetes and osteoporosis has been extensively investigated. However, whether the effects of HS on osteoblast function under high glucose (HG) condition relate to ATP-sensitive potassium (KATP) channels is unclear. This study aimed to investigate the effects of HS on the proliferation, apoptosis, and mineralization of osteoblasts under HG condition, and observe whether HS 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 HS 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, the expression of KATP SUR1 was also determined. NaHS pretreatment significantly inhibited the 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. HS prevents the HG-induced osteoblast damage through regulating KATP channels.