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

Abstract

Objective

The protective effects of epigallocatechin gallate (EGCG) on interleukin-1β (IL-1β)-induced apoptosis were investigated in murine MIN₆ pancreatic β-cells. The role of uncoupling protein-3 (UCP₃) signaling in this process was also explored.

Methods

After treatment with IL-1β and EGCG, cells were collected and analyzed. Cell viability was measured using the CCK₈ assay and the function of β-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-1β 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-1β-induced apoptosis (p<0.01), restored mitochondrial function and subsequently increased UCP₃ levels in IL-1β-induced β-cells (p<0.01).

Conclusion

These results suggest that EGCG protects against IL-1β-induced mitochondrial injury and apoptosis in β-cells through the up-regulation of UCP₃.

Keywords:

• EGCG
• pancreatic β-cells
• apoptosis
• UCP₃

Acknowledgments

This work was supported by Key project of Sichuan Province Department of Education, China (17ZA0168, 17ZA0167); Special Project of Strategic Cooperation in Nanchong City, China (18SXH20224)

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors do not have potential financial conflicts of interest related to this manuscript. The authors report no conflicts of interest for this work.