Gallic Acid and Gallic Acid Nanoparticle Modulate Insulin Secretion Pancreatic β-Islets against Silica Nanoparticle-Induced Oxidative Damage

Due to the increasing use of silica nanoparticles (SiNPs), their possible toxic effects on human health have undoubtedly been considered. Previous studies proved that SiNPs induced oxidative stress. Reactive oxygen species (ROS) and oxidative stress disrupt cell function and decrease insulin secretion. Therefore, this study intended to assess the effects of SiNPs on oxidative stress and insulin secretion and also the protective effects of gallic acid (GA) and gallic acid nanoparticles (NP-GA) on pancreatic beta-islets. In this study, the mice islets were separated and pretreated with various concentrations of GA and NP-GA then treated with a single dose of SiNPs. The cell viability of islets examined by MTT assay and also the levels of ROS, malondialdehyde (MDA), glutathione (GSH); activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and insulin secretion were evaluated. The results of MTT assay showed that SiNPs reduced islet viability in a dose-dependent manner and also insulin secretion, induced the formation of ROS, augmented MDA amounts, and decreased GSH levels, SOD, GPx, and CAT activities. Furthermore, pretreatment of islets with GA and NP-GA significantly returned these alterations at low dose. These findings suggested that SiNPs induced oxidative stress in the pancreatic islets, which could be one of the reasons for the decrease in insulin secretion and inducing diabetes. This study also showed that low doses of GA and NP-GA boosted the antioxidant defense system in the pancreatic beta-islets, preventing oxidative stress and, consequently, the progression of diabetes.

Automated summary

SiNPs induce oxidative stress in pancreatic islets, leading to decreased insulin secretion and diabetes, while GA and NP-GA can protect pancreatic islets from oxidative stress.