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没食子酸和没食子酸纳米粒子调节胰岛素分泌胰岛β细胞对抗二氧化硅纳米颗粒诱导的氧化损伤。

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

机构信息

Health Research Institute, Diabetes Research Center, Department of Physiology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Department of Toxicology, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

出版信息

Biol Trace Elem Res. 2022 Dec;200(12):5159-5171. doi: 10.1007/s12011-022-03111-y. Epub 2022 Jan 12.

Abstract

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 β-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 β-islets, preventing oxidative stress and, consequently, the progression of diabetes.

摘要

由于二氧化硅纳米粒子(SiNPs)的使用越来越多,它们对人类健康可能产生的毒性作用无疑已受到关注。先前的研究证明 SiNPs 会引起氧化应激。活性氧(ROS)和氧化应激会破坏细胞功能并减少胰岛素分泌。因此,本研究旨在评估 SiNPs 对氧化应激和胰岛素分泌的影响,以及没食子酸(GA)和没食子酸纳米粒子(NP-GA)对胰腺β-胰岛的保护作用。在这项研究中,将小鼠胰岛分离出来,用不同浓度的 GA 和 NP-GA 进行预处理,然后用单剂量的 SiNPs 处理。通过 MTT 测定法检查胰岛的细胞活力,还评估了 ROS、丙二醛(MDA)、谷胱甘肽(GSH)的水平;超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)的活性以及胰岛素分泌。MTT 测定法的结果表明,SiNPs 以剂量依赖性方式降低胰岛活力,并且还降低胰岛素分泌,诱导 ROS 的形成,增加 MDA 含量,降低 GSH 水平、SOD、GPx 和 CAT 活性。此外,用 GA 和 NP-GA 预处理胰岛可在低剂量时显著恢复这些变化。这些发现表明,SiNPs 诱导了胰腺胰岛的氧化应激,这可能是胰岛素分泌减少和引发糖尿病的原因之一。本研究还表明,GA 和 NP-GA 的低剂量可增强胰腺β-胰岛的抗氧化防御系统,防止氧化应激,从而阻止糖尿病的发展。

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