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DOI 10.7518/hxkq.2017.05.005

Медицинская библиотека · Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2017

[Role of adenosine triphosphate-sensitive potassium channel in hydrogen sulfide-induced inhibition of high glucoseinduced osteoblast damage].

Yuanyuan Liu, Xiumei Guan, Min Cheng, Xin Li, Yueyang Pan, Zhiliang Guo

СтатьяПеревод в очереди

Аннотация

OBJECTIVE

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

Through the KATP channel, H₂S inhibited osteoblasts damage induced by HG.

Для цитирования: Yuanyuan Liu, Xiumei Guan, Min Cheng, Xin Li, Yueyang Pan, Zhiliang Guo. [Role of adenosine triphosphate-sensitive potassium channel in hydrogen sulfide-induced inhibition of high glucoseinduced osteoblast damage].. Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology. 2017. DOI: 10.7518/hxkq.2017.05.005.

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