| Diabetes can be divided into type 1 diabetes and type 2 diabetes, which is one of the major diseases risks to human health. Autoimmune attacking, inflammatory factors and glucolipotoxicity induced pancreaticβcell apoptosis play a key role in onset and development of both diabetes types. Therefore, the study of abnormal pancreaticβcell apoptosis mechanism, and further, find ways to protectβcell apoptosis will provide important guidance for diabetes treatment.In this study, we chose in vitro cultured mouse pancreaticβcell lines as experimental material, incubated these cell lines with inflammatory cytokines IL-1β,IFNγ,and high concentration of glucose,palmitate to imitate in vivo diabetes patient environment, analyzed prolactin's protective effect on pancreaticβcell apoptosis. We found that prolactin can significantly protect pancreaticβcell from inflammatory cytokines and high glucose and palmitate induced apoptosis, and this protective effect is related to Jak2-STAT5 signaling pathway activation. Using Jak2 specific inhibitor AG490 block Jak2 protein kinase activity could significantly inhibit the protective effect of prolactin caused by glucolipotoxicity. In addition, our study found that high concentration of high glucose and palmitate induce pancreaticβcell endoplasmic reticulum stress, while prolactin can completely rescue endoplasmic reticulum stress caused by glucolipotoxicity, which may explain its protective role ofβcell apoptosis. |