Role of adenosine triphosphate-sensitive potassium channel in hydrogen sulfide-induced inhibition of high glucoseinduced osteoblast damage / 华西口腔医学杂志

<p><b>OBJECTIVE</b>The aim of this study is to identify the role of adenosine triphosphate-sensitive potassium channel (KATP) in hydrogen sulfide (H₂S)-induced inhibition of high glucose (HG)-induced osteoblast damage.</p><p><b>METHODS</b>Osteoblasts from rat mandible were cultured and identified. The osteoblasts were then treated with HG, H₂S, KATP channel opener pinacidil (Pia), and KATP channel blocker glibenclamide (Gli). Western blot method was performed to detect the expression of KATP channel protein. CCK8, reverse transcriptase polymerase chain reaction (RT-PCR) , and image analysis were used to determine the effects of H₂S-KATP on the proliferation, differentiation, and mineralization of osteoblasts.</p><p><b>RESULTS</b>The expression of KATP channel protein in osteoblasts was significantly decreased under the influence of HG. H₂S pretreatment significantly inhibited HG on KATP channel protein down-regulation. Moreover, H₂S pretreatment significantly inhibited the effect of HG on the proliferation of osteoblasts, thereby preventing HG-induced inhibition of osteoblasts differentiation and mineralization. Meanwhile, the KATP channel blocker effectively blocked the H₂S on osteoblasts and had a protective effect.</p><p><b>CONCLUSIONS</b>Through the KATP channel, H₂S inhibited osteoblasts damage induced by HG.</p>

The inhibition of genistein on proliferation and transcription of c-fos mRNA in human umbilical vascular smooth muscle cells induced by MCP-1 / 中国药理学通报

Aim To study the inhibition of genistein on proliferation and transcription of c-fos mRNA in human umbilical vascular smooth muscle cells(hUVSMC) induced by monocyte chemotactic protein-1(MCP-1). Methods Growth-arrested hUVSMC were stimulated with MCP-1(10 ?g?L-1) prior to co-treatment with different concentrations of genistein (10,30,90 ?mol?L-1). The response of hUVMSC to these treatments was observed in comparison with that of control group. The proliferation of hUVMSC was evaluated by cell counting. The expression of c-fos mRNA was detected by RT-PCR. Results Low concentration of genistein(10 ?mol?L-1) inhibited the proliferation of hUVSMC and high concentration of genistein(30,90 ?mol?L-1) inhibited the expression of c-fos in hUVSMC induced by MCP-1. Conclusions Genistein could suppress the proliferation of hUVSMC induced by of MCP-1. Its mechanisms may involve the down-regulation of c-fos mRNA expression.