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Journal of Ophthalmology
Volume 2017 (2017), Article ID 7205408, 10 pages
Research Article

The Protective Effects of αB-Crystallin on Ischemia-Reperfusion Injury in the Rat Retina

1Department of Ophthalmology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
2Chongqing Aier-Mega Eye Hospital, Aier Eye Hospital Group, Chongqing 400060, China

Correspondence should be addressed to Li Li

Received 24 April 2017; Revised 28 July 2017; Accepted 6 August 2017; Published 2 October 2017

Academic Editor: Jesús Pintor

Copyright © 2017 Huan Yan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To investigate whether αB-crystallin protects against acute retinal ischemic reperfusion injury (I/R) and elucidate the potential antioxidant mechanisms. Retinal I/R injury was made by elevating the intraocular pressure (IOP) 110 mmHg for 60 min, and αB-crystallin (1 × 10−5 g/L) or vehicle solution was administered intravitreously immediately after I/R injury. The animal was sacrificed 24 h, 1 w, and 1 m after the I/R injury. The retina damage was detected by hematoxylin and eosin (HE) staining and electroretinography (ERG). The level of malondialdehyde (MDA), nitric oxide (NO), and the total superoxide dismutase (T-SOD) was determined. An immunohistochemical study was performed to detect the activation of inducible nitric oxide synthase (iNOS) and NF- (nuclear factor-) kappaB (NF-κB) p65. The decrease of retinal thickness and the number of retinal ganglion cells (RGCs) can be suppressed by αB-crystallin. And the amplitudes of a- and b-wave were remarkably greater without αB-crystallin. Similarly, αB-crystallin also significantly decreased the level of MDA and NO and enhanced the activities of T-SOD. The positive expression of iNOS and NF-kappaB p65 was obviously reduced while treated with αB-crystallin. αB-crystallin can inhibit the expression of NF-κB and its antioxidative effect to protect the retina from I/R injury.