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

Huan Yan,Liyan Gong,Li Li,Yanli Peng,Wei Huang

doi:10.1155/2017/7205408

Abstract

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.

Highlights

Retinal ischemia reperfusion (I/R) injury is responsible for several vision-threatening ocular diseases such as retinal vascular occlusion, acute glaucoma, diabetic retinopathy, and retinopathy of prematurity [1, 2]
The results showed that αB-crystallin could decrease the loss of retinal ganglion cells (RGCs) and prevent inner plexiform layer (IPL), inner nuclear layer (INL), and outer nuclear layers (ONL) from becoming thinner
We have demonstrated that αB-crystallin had a neuroprotective effect on the retina after ischemia reperfusion injury through its antioxidant activities and achieved by inhibiting the expression of NF-κB

Summary

Introduction

Retinal ischemia reperfusion (I/R) injury is responsible for several vision-threatening ocular diseases such as retinal vascular occlusion, acute glaucoma, diabetic retinopathy, and retinopathy of prematurity [1, 2]. ΑB-crystallin is a prominent member of the small heatshock protein family, which has been documented to distribute in different tissues such as lens, neural retina, retinal pigment epithelium, heart, skeletal muscle, kidney, and brain [4,5,6]. ΑB-crystallin is not solely recognized in chaperone effect, it includes antiangiogenesis and antioxidative stress [7,8,9]. Nowadays, emerging evidences demonstrate that αB-crystallin retrieves organs and tissues from the impairment of I/R, including the heart and brain [10, 11]. There is few research concerning the effect of αB-crystallin to protect retina from the damage of I/R

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