| ObjectiveTo explore the relationship between the expression of Bcl-2/Bax and cellapoptosis in retinal ischemia reperfusion (IR)injury of rats,as well as thetherapeutic effects of hydrogen sulfide in ischemia retina.MethodThe model of retinal ischemia-reperfusion injury was made by transientelevating introcular pressure.We used sodium hydrosulfide(NaHS) as the donorof hydrogen sulfide. A total of54SD rats were randomly divided into nomalcontrol group,ischemia-reperfusion model group and sodium hydrosulfidetreetment group,the last two group were subdivided in group6hours,24hours,48hours,72hours after reperfusion.The models of retinalischemia-reperfusion injury were made by elevating intraocularpressure.Apoptosis was assessed by the term in aldeoxy nucleotidyltransferase mediated dUTP nick end labelling method,and the expression ofBcl-2/Bax was studied by immunohis to chemistry.ResultThe normal rat retinal organizational structure was clear and complete,andhad no apoptotic cells.Ischemia-reperfusion group,with the reperfusion timeincreased,retinal damage was gradually increased.In the inner retina appearededema,interstitial gradually shrinking.Beginning level unclear.Retinal ganglioncell and inner nuclear layer loosely arranged and disorder,and reduce.Some cells pyknosis,dissolve,necrosis.Disordered and cytoplasm vacuolatedchanges,lighten the retinal edema after48hours.Retinal structure returned tonormal after72hours,then,retina thinned.Of H2S in the intervention grouptrends and retinal histological changes similar to ischemia-reperfusion group,butat all levels are to some extent the thickness of recovery,cell loss,vacuolardegeneration.At the ischemia-reperfusion group,the expression of apoptosisbegan to increase at6hours after reperfusion.The number of apoptotic cellsreached the peak at24hours after ischemia,then decrease gradually.Noexpression of Bcl-2and Bax positive cells were found in normal group,at theischemia-reperfusion groups,the expression of Bcl-2reached the peak at6hours after reperfusion.Began to decrease at24hours,and weakened obviouslyat72hours.The expression of Bax began to increase at6hours afterreperfusion.At24hours reached the peak, began to decrease at48hours,andweakened obviously at72hours.The therapy groups of hydrogen sulfide havethe same trend with the ischemic groups in each index. H2S in the interventiongroup reduced apoptotic cells and Bax protein expression decreased and Bcl-2protein expression increased significantly in the H2S intervention group againstischemia-reperfusion group.Between the two groups was statistically significantdifference(P<0.05).ConclusionRIRI mainly damage the inner retinal.Bcl-2and Bax play an important role inthe happening of RIRI. H2S can enhance the expression of Bcl-2,decrease theexpression of Bax, increase the Bcl-2/Bax ratioand decrease the apoptosis ofganglion cells. H2S shows a significant protection for retinal ganglion cells withRIRI. |
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