Resveratrol Ameliorates Retinal Ischemia/Reperfusion Injury in C57BL/6J Mice via Downregulation of Caspase-3

• Published in: Current eye research Vol. 42; no. 12; pp. 1650 - 1658
• Main Authors: Seong, Hyemin, Ryu, Jinhyun, Yoo, Woong-Sun, Kim, Seong Jae, Han, Yong-Seop, Park, Jong Moon, Kang, Sang Soo, Seo, Seong Wook
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 02.12.2017
• Subjects: Animals; Antioxidants - pharmacology; Apoptosis - drug effects; Blotting, Western; Caspase 3 - genetics; Caspase 3 - metabolism; Caspase 8 - genetics; Caspase 8 - metabolism; Caspase-3; caspase-8; Disease Models, Animal; Down-Regulation; Gene Expression Regulation, Enzymologic - physiology; In Situ Nick-End Labeling; Injections, Intraperitoneal; ischemia/reperfusion injury; Male; Mice; Mice, Inbred C57BL; Real-Time Polymerase Chain Reaction; Reperfusion Injury - enzymology; Reperfusion Injury - pathology; Reperfusion Injury - prevention & control; resveratrol; retina; Retinal Degeneration - enzymology; Retinal Degeneration - pathology; Retinal Degeneration - prevention & control; RNA, Messenger - genetics; Stilbenes - pharmacology; caspase-8; ischemia/reperfusion injury; retina; Caspase-3; resveratrol
• ISSN: 0271-3683; 1460-2202
• DOI: 10.1080/02713683.2017.1344713

Purpose: Ischemia/reperfusion (I/R) injury induces apoptosis in retinal ganglion cells (RGCs). Resveratrol (Res) is a potent natural antioxidant with beneficial effects in many ocular diseases, such as age-related macular degeneration, diabetic retinopathy, and glaucoma. Because caspase-3 expression is highly correlated with activation of the apoptotic pathway, the present study aimed to determine whether Res regulates the expression of caspase-3 using an I/R retinal injury mouse model. Methods: Male C57BL/6J mice were injected with Res for 2 consecutive days before I/R retinal injury. I/R retinal injury was induced by increasing the intraocular pressure for 1 h. Res was then injected for 3 consecutive days. Changes in retinal morphology were monitored for 3 days after injury by histochemistry using hematoxylin and eosin staining. mRNAs and proteins were extracted 2 days after injury. The expression levels of caspase-8 and caspase-3 mRNA and protein were determined using reverse-transcriptase polymerase chain reaction (RT-PCR) and western blot analyses. Results: I/R injury induced declines in retinal thickness and number of RGCs during 5 days after injury. Caspase-8 and caspase-3 mRNA and protein activation increased. Res treatment reduced the significant loss of retinal morphology and downregulated the expression of mRNA and activation of caspase-8 and caspase-3 protein. Conclusions: The observed changes in retinal morphology suggest that I/R injury promotes retinal degeneration. Increased expression of caspase-8 and caspase-3 mRNA indicates apoptosis activation. Res, however, suppresses apoptosis via downregulation of caspase-8 and caspase-3 expression.