Silencing information regulator (SIRT1) involves in endocrine diseases. However, whether SIRT1 participates in BMSCs under high glucose environment remains unclear. Rat BMSCs were isolated and divided into control group; high glucose group; and SIRT1 group, in which SIRT1 agonist (Resveratrol)
was added to high glucose BMSCs followed by analysis of SIRT1, Bax and Bcl-2 expression by real time PCR and ELISA, cell proliferation by MTT assay, Caspase3 activity, ALP activity, calcification nodule formation by alizarin red staining, changes of ROS and SOD activities, PI3K signaling pathway
by Western blot. SIRT1 expression was significantly decreased in BMSCs in high glucose group, with inhibited cell proliferation, increased Caspase 3 activity, Bax expression, and ROS content, decreased Bcl-2 expression, ALP activity, SOD activity, as well as reduced formation of calcified
nodules and phosphorylation of PI3K compared to control (P < 0.05). Addition of Resveratrol significantly promoted SIRT1 expression and cell proliferation of BMSCs in high glucose group, decreased Caspase 3 activity, Bax expression, and ROS content, increased Bcl-2 expression, ALP
activity, SOD activity, as well as increased formation of calcified nodules and phosphorylation of PI3K (P < 0.05). SIRT1 expression is decreased in BMSCs in high glucose group. Increasing SIRT1 expression in BMSCs under high glucose environment promoted proliferation of BMSCs and the formation
of calcified nodules by regulating oxidative stress and activating PI3K signaling pathway.