Non-receptor tyrosine kinase inhibitors enhances β-cell survival by suppressing the PKCδ signal transduction pathway in streptozotocin-induced β-cell apoptosis.

摘要: GNF-2 and GNF-5 are members of a new class non-receptor tyrosine kinases inhibitors that possess excellent selectivity towards imatinib-resistant mutations found in chronic myeloid leukemia patients. On the other hand recent reports implicate abnormal kinase signaling β-cell death Type I II diabetes. In this work we determined effects GNF-2, on pancreatic caused by streptozotocin (STZ). STZ treatment causes apoptosis INS-1 cells activation intracellular ROS, c-jun N-terminal (JNK), caspase 3, 3-dependent protein C delta (PKCδ). increased cell viability attenuated STZ-induced ROS significantly reduced JNK, PKCδ. studies with intact mice, GFN-2 prevented loss beta increase blood glucose produced STZ-treated control mice. Furthermore, immunohistochemical analysis revealed insulin levels mice when compared These findings suggest provide approach for new-onset