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Gastrodin inhibits high glucose‑induced human retinal endothelial cell apoptosis by regulating the SIRT1/TLR4/NF‑κBp65 signaling pathway.
- Source :
-
Molecular medicine reports [Mol Med Rep] 2018 Jun; Vol. 17 (6), pp. 7774-7780. Date of Electronic Publication: 2018 Apr 03. - Publication Year :
- 2018
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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.
- Subjects :
- Cell Survival drug effects
Glucose metabolism
Humans
Oxidative Stress drug effects
Reactive Oxygen Species metabolism
Retina cytology
Retina metabolism
Signal Transduction drug effects
Apoptosis drug effects
Benzyl Alcohols pharmacology
Endothelial Cells drug effects
Endothelial Cells metabolism
Glucosides pharmacology
Sirtuin 1 metabolism
Toll-Like Receptor 4 metabolism
Transcription Factor RelA metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-3004
- Volume :
- 17
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Molecular medicine reports
- Publication Type :
- Academic Journal
- Accession number :
- 29620267
- Full Text :
- https://doi.org/10.3892/mmr.2018.8841