| Objectives:alpha B-crystallin（αB-crystallin）is a member of the small heat shock protein family,which nowadays has been documented to retrieve organs and tissues from the impairment of I/R.We at present investigate whetherαB-crystallin protects against acute retinal ischemic reperfusion injury（I/R）,and elucidate the potential antioxidant mechanisms.Methods:72 Adult male Sprague-Dawley rats were randomly divided into three groups:sham,I/R plus vehicle,and I/R plusαB-crystallin.Retinal I/R injury was made by elevating the intraocular pressure（IOP）110mmHg for 60 min,after whichαB-crystallin(1×10-5g/L)or vehicle solution was administered intravitreously immediately.The animal was sacrificed 24h,1w and 1m after the I/R injury.The retina damage was detected by hematoxylin and eosin（HE）staining and Electroretinography（ERG）.Furthermore,the level of malondialdehyde（MDA）,nitric oxide（NO）and the total superoxide dismutase（T-SOD）was determined.An immunohischemical study was performed to detect the activation of inducible nitric oxide synthase（iNOS）and NF（nuclear factor）-kappaB p65（NF-κB）.Results:Our study suggested thatαB-crystallin significantly suppressed the decrease of retinal thickness including the inner nuclear layer（INL）,inner plexiform layer（IPL）,and outer nuclear layer（ONL）as well as the number of cells in the ganglion cell layer（GCL）.And in I/R plusαB-crystallin group,the amplitudes of a-and b-wave were remarkably greater than I/R plus vehicle group（P<0.05）.Similarly,αB-crystallin also significantly decreased the level of MDA and NO,and enhanced the activities of T-SOD.Compared with I/R plus vehicle group,the positive expression of iNOS and NF-kappaB p65 was obviously reduced while treated withαB-crystallin.Conclusions:αB-crystallin can protect the retina from I/R injury,possibly through anti-oxidative mechanism and by inhibiting the expression of NF-κB. |
