Gomisin N Improves Insulin Secretion by Alleviating Endoplasmic Reticulum and Oxidative Stress in Pancreatic Beta Cells.

Abstract

This study investigated the effects of gomisin N (25 μM) using a cyclopiazonic acid (CPA, 50 μM)-induced injury model of MIN6 pancreatic beta-cells. The results demonstrated that gomisin N effectively reduced the expression of endoplasmic reticulum (ER) stress markers that were increased by CPA. Furthermore, gomisin N treatment improved insulin secretion from MIN6 cells, which had been reduced by CPA. These findings suggest that alleviation of ER stress and oxidative stress ultimately supports the correct folding and maturation of insulin precursors and enhances beta-cell viability, leading to functional normalization. Gomisin N exhibited antioxidant effects by significantly reducing reactive oxygen species (ROS) levels that were increased by CPA. Given that ER stress and oxidative stress are closely linked and cooperatively drive cellular damage, the dual stress-relieving properties of gomisin N are critical for beta-cell protection. By alleviating ER stress and reducing oxidative stress, gomisin N acts to protect and restore insulin secretory function in beta-cells. Therefore, gomisin N could play a beneficial role in protecting and improving pancreatic beta-cell function, particularly under stress conditions.