| Objective: To investigate the neuroprotective effect and mechanism of betaxolol on experimental retinal ischemia-reperfusion injury.Method: Retinal ischemia was induced in SD rats by increasing intraocular pressure to 110mmHg for 60 minutes. The 56 rats were divided into normal control group (N,eight rats), Ischemic Reperfusion +0.25% Betaxolol treatment group (I/R+BE, twenty-four rats) and Ischemic Reperfusion+ normal saline control (I/R+NS, twenty-four rats) group randomly,The latter two groups were subdivided into group 1 day,3 and 7 days after reperfusion respectively,and with 8 rats in each group. 0.25% Betaxolol was applied to I/R+BE group and normal saline to I/R+NS group at the beginning of reperfusion and then again, twice daily (9-10a.m.and8-9p.m.)for 1,3 or 7 days after reperfusion.At those time points,The electroretinography(ERG) b-wave and the histological and ultrastructural changes in retina of each group were observed.The expression of nNOS was studied by immunocytochemistry.Result: In the different reperfusion time,the histopathologic damages of retina in I/R+NS group were more serious compared with I/R+BE group;the amplitudes of ERG b-wave recovery was significantly higher in I/R+BE group ( 57.24 ± 4.54 , 73.77 ± 9.33 , 89.23 ± 6.75 ) than that of I/R+NS group ( 32.13 ± 7.28 , 23.91 ± 2.77,16.51 ± 8.38 ) ( P<0.01 ) ;the nNOS immunoreactive cells were located to the inner nuclear layer (INL) and the ganglion cell layer (GCL) of normal retina, 1 day after reperfusion,the number of nNOS-located cells started to increase in both GCL and INL of I/R+NS group,which persisted up to 3 days after reperfusion,I/R+BE group had ( 0.657 ± 0.013 , 0.684 ± 0.058 , 0.670 ± 0.026 ) fewer nNOS-positive cells than I/R+NS group had( 1.573 ± 0.353,3.740 ± 0.118,2.460 ± 0.603 ) (P<0.01).Conclusion: Betaxolol, by reducing Calcium influx and NO production,can protect retina neurons from injury associated with ischemia/reperfusion. |
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