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

Authors Jia X, Luo Z, Gao Y, Liu H, Liu X, Mai W, Liu H, Zheng Q

Received 1 July 2020

Accepted for publication 6 September 2020

Published 13 October 2020 Volume 2020:14 Pages 4251—4261

DOI https://doi.org/10.2147/DDDT.S270345

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yan Zhu


Xu Jia,1,* Ziren Luo,2,* Ying Gao,3 Hua Liu,3 Xinghai Liu,3 Wenli Mai,3 Hong Liu,3 Qian Zheng3

1Department of Pharmacy, Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, People’s Republic of China; 2School of Pharmacy, North Sichuan Medical College, Nanchong 637000, People’s Republic of China; 3Department of Physiology, North Sichuan Medical College, Nanchong 637007, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Qian Zheng
Department of Physiology, North Sichuan Medical College, Nanchong, 637007, People’s Republic of China
Email 373969568@qq.com

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

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