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Hydroxysafflor yellow A attenuates high glucose-induced pancreatic β-cells oxidative damage via inhibiting JNK/c-jun signaling pathway

Author:
Zhao, Ying, Sun, Hanchen, Li, Xiaosai, Zha, Yumei, Hou, Weikai
Source:
Biochemical and biophysical research communications 2018 v.505 no.2 pp. 353-359
ISSN:
0006-291X
Subject:
Western blotting, acetylcysteine, apoptosis, catalase, fluorescence microscopy, glucose, glutathione peroxidase, insulin secretion, islets of Langerhans, lipid peroxidation, mitogen-activated protein kinase, models, oxidative stress, proteins, quantitative polymerase chain reaction, rats, reactive oxygen species, reverse transcriptase polymerase chain reaction, signal transduction, superoxide dismutase, therapeutics, toxicity
Abstract:
Pancreatic β-cells apoptosis and dysfunction induced by glucose toxicity were attributed to the formation of excess oxidative damage. Some studies have found that hydroxysafflor yellow A has strong effects to scavenge oxidative stress and inhibit apoptosis. In order to explore the influence of HSYA on oxidative stress induced by high glucose and the potential mechanisms, we set up a high glucose damage model and induced oxidative stress in INS-1 rat insulinoma cells. N-acetylcysteine was added as a group of oxidative stress scavenger. After 72 h of cultivation, the related indexes of oxidative stress (reactive oxygen species, catalase, glutathione peroxidase, lipid peroxidation, and superoxide dismutase), apoptosis (caspase3, parp) and the function of glucose stimulated insulin secretion were determined. In addition, the signaling pathway proteins of C-Jun NH2 -terminal kinases (JNK), phosphorylated JNK, C-jun, phosphorylated C-jun were evaluated. Fluorescence microscopy, qRT-PCR, western blotting were the main methods used in the experiment. Our results showed that hydroxysafflor yellow A reduced pancreatic β-cells apoptosis by attenuating oxidative damage, and JNK/c-Jun signaling pathway was involved. It indicated a significant mechanism for the positive impacts of HSYA on oxidative stress induced by high glucose, and provide important basis for using HSYA in diabetic prevention and therapy.
Agid:
6153541