EGCG Upregulates UCP3 Levels to Protect MIN6 Pancreatic Islet Cells from Interleukin-1β-Induced Apoptosis

Objective: The protective effects of epigallocatechin gallate (EGCG) on interleukin-1 beta (IL-1 beta)-induced apoptosis were investigated in murine MIN6 pancreatic beta-cells. The role of uncoupling protein-3 (UCP3) signaling in this process was also explored. Methods: After treatment with IL-1 beta and EGCG, cells were collected and analyzed. Cell viability was measured using the CCK8 assay and the function of beta-cells was evaluated by analyzing insulin secretion. Detection of mitochondrial function in cells was performed by measuring mitochondrial membrane potential, the concentration of ATP and activity of ROS. Apoptosis was analyzed by Hochest33258 staining and flow cytometry. Expression levels of UCP3 were interrogated using immunohistochemistry, RT-PCR and Western blotting. Results: Compared with the control group, IL-1 beta treatment (20nM) for 24 h significantly decreased cell viability and insulin secretion, damaged mitochondrial function and increased ROS activity. Results also showed increased apoptosis and a decrease in UCP3 expression levels (p<0.01). However, treatment with low (1mM) or high (5mM) concentrations of EGCG significantly decreased IL-1 beta-induced apoptosis (p<0.01), restored mitochondrial function and subsequently increased UCP3 levels in IL-1 beta-induced beta-cells (p<0.01). Conclusion: These results suggest that EGCG protects against IL-1 beta-induced mitochondrial injury and apoptosis in beta-cells through the up-regulation of UCP3.