Objective To investigate the effects of GDF11 on apoptosis of BMSCs from diabetic mice and the related mechanism.Methods BMSCs of normal mice (Nor),diabetic mice (DB),DB with GDF11 intervention (GDF11),and DB+GDF11 plus LY294002 (LY) were cultured for 3 days.Trypan blue staining was used to calculate the apoptotic rate,while western blot was used to investigate protein levels of Bax,Bcl-2,phosphorylated (p)-PI3K and p-Akt.Results Compared with Nor,the apoptotic rate of DB was increased [(36.2±3.3)% vs. (3.1±1.1)%,P＜0.05],but GDF11 intervention could reduce the apoptotic rate [(18.9±1.9)% vs. (36.2±3.3)%,P＜0.05],increase Bcl-2/Bax expression[(1.63±0.10) vs. (0.26±0.09);P＜0.05],and activate the PI3K[p-PI3K/PI3K:(0.98±0.08) vs. (0.42±0.11);P＜0.05]/Akt[p-Akt/Akt:(0.94±0.10) vs. (0.32±0.15);P＜0.05]signaling pathway.However,when inhibiting PI3K/Akt signaling pathway,GDF11 had its inhibitory effect on cell apoptosis blunted[apoptotic rate:(41.1±3.9)% vs. (18.9±1.9)%,P＜0.05].Conclusions GDF11 can inhibit the apoptosis of BMSCs from diabetic mice by activating the PI3K/Akt signaling pathway.
Key words
DGF11 /
diabetes /
bone-marrow mesenchymal stem cells (BMSCs) /
cell apoptosis
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