Gastrodin inhibits high glucose-induced human retinal endothelial cell apoptosis by regulating the SIRT1/TLR4/NF-κBp65 signaling pathway

Abstract

Diabetic retinopathy (DR), one of the most common complications of late-phase diabetes, is associated with the ectopic apoptosis of microvascular cells. Gastrodin, a phenolic glucoside derived from Gastrodia elata Blume, has been reported to have antioxidant and anti-inflammation activities. The aim of the present study was to investigate the effects of gastrodin on high glucose (HG)-induced human retinal endothelial cell (HREC) injury and its underlying mechanism. The results demonstrated that HG induced cell apoptosis in HRECs, which was accompanied by increased levels of reactive oxygen species production. Gastrodin treatment significantly alleviated HG-induced apoptosis and oxidative stress. Furthermore, HG stimulation decreased the levels of SIRT1, which was accompanied by an increase in Toll-like receptor 4 (TLR4) expression and the levels of phosphorylated nuclear factor (NF)-κBp65. However, the administration of gastrodin significantly inhibited the activation of the sirtuin 1 (SIRT1)/TLR4/NF-κBp65 signaling pathway in HRECs exposed to HG. Collectively, the present study demonstrated that gastrodin may be effective against HG-induced apoptosis and its action may be exerted through the regulation of the SIRT1/TLR4/NF-κBp65 signaling pathway.