PMID- 31345961 OWN - NLM STAT- MEDLINE DCOM- 20200909 LR - 20200909 IS - 1573-4935 (Electronic) IS - 0144-8463 (Print) IS - 0144-8463 (Linking) VI - 39 IP - 8 DP - 2019 Aug 30 TI - Protective effects of delphinidin against H(2)O(2)-induced oxidative injuries in human retinal pigment epithelial cells. LID - BSR20190689 [pii] LID - 10.1042/BSR20190689 [doi] AB - Age-related macular degeneration (AMD) is now one of the leading causes of blindness in the elderly population and oxidative stress-induced damage to retinal pigment epithelial (RPE) cells occurs as part of the pathogenesis of AMD. In the present study, we evaluated the protective effect of delphinidin (2-(3,4,5-trihydroxyphenyl) chromenylium-3,5,7-triol) against hydrogen peroxide (H(2)O(2))-induced toxicity in human ARPE-19 cells and its molecular mechanism. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and flow cytometry demonstrated that pretreatment of ARPE-19 cells with delphinidin (25, 50, and 100 mug/ml) significantly increased cell viability and reduced the apoptosis from H(2)O(2) (0.5 mM)-induced oxidative stress in a concentration-dependent manner, which was achieved by the inhibition of Bax, cytochrome c, and caspase-3 protein expression and enhancement of Bcl-2 protein. The same tendency was observed in ARPE-19 cells pre-treated with 15 mM of N-acetylcysteine (NAC) before the addition of H(2)O(2) Furthermore, pre-incubation of ARPE-19 cells with delphinidin markedly inhibited the intracellular reactive oxygen species (ROS) generation and Nox1 protein expression induced by H(2)O(2) Moreover, the decreased antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GSH-PX) and elevated (MDA) level in H(2)O(2)-treated cells were reversed to the normal standard by the addition of delphinidin, which was regulated by increasing nuclear Nrf2 protein expression in ARPE-19 cells. Our results suggest that delphinidin effectively protects human ARPE-19 cells from H(2)O(2)-induced oxidative damage via anti-apoptotic and antioxidant effects. CI - (c) 2019 The Author(s). FAU - Ni, Timin AU - Ni T AD - Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan 430060, China. AD - Department of Ophthalmology, Wuhan Central Hospital, Wuhan 430014, China. FAU - Yang, Wanju AU - Yang W AD - Department of Ophthalmology, Wuhan Central Hospital, Wuhan 430014, China. FAU - Xing, Yiqiao AU - Xing Y AUID- ORCID: 0000-0002-0980-1598 AD - Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan 430060, China yiqiaoxingwuhan@gmail.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20190815 PL - England TA - Biosci Rep JT - Bioscience reports JID - 8102797 RN - 0 (Anthocyanins) RN - BBX060AN9V (Hydrogen Peroxide) RN - EM6MD4AEHE (delphinidin) SB - IM MH - Anthocyanins/*pharmacology MH - Cell Line MH - Epithelial Cells/*metabolism/pathology MH - Humans MH - Hydrogen Peroxide/*pharmacology MH - Oxidative Stress/*drug effects MH - Retinal Pigment Epithelium/*injuries/*metabolism/pathology PMC - PMC6695502 OTO - NOTNLM OT - Age-related macular degeneration OT - Antioxidant OT - Apoptosis OT - Delphinidin OT - Human retinal pigment epithelial cells OT - Oxidative stress COIS- The authors declare that there are no competing interests associated with the manuscript. EDAT- 2019/07/28 06:00 MHDA- 2020/09/10 06:00 PMCR- 2019/08/15 CRDT- 2019/07/27 06:00 PHST- 2019/03/20 00:00 [received] PHST- 2019/06/20 00:00 [revised] PHST- 2019/07/14 00:00 [accepted] PHST- 2019/07/28 06:00 [pubmed] PHST- 2020/09/10 06:00 [medline] PHST- 2019/07/27 06:00 [entrez] PHST- 2019/08/15 00:00 [pmc-release] AID - BSR20190689 [pii] AID - 10.1042/BSR20190689 [doi] PST - epublish SO - Biosci Rep. 2019 Aug 15;39(8):BSR20190689. doi: 10.1042/BSR20190689. Print 2019 Aug 30.