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首页> 外文期刊>Cellular Physiology and Biochemistry >The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina
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The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

机译：Rho激酶抑制的神经保护潜力，促进孤立的牛视网膜缺氧反应中促进细胞存活和减少反应性胶质变性。

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biAims /i/bTo investigate the outcomes of Rho-kinase inhibition in the electrophysiological iex vivo/i model of the isolated perfused vertebrate retina under hypoxia. biMethods /i/bBovine retinas were perfused with an oxygen saturated nutrient solution with or without the Rho-kinase inhibitor H-1152P. The retinas were stimulated repeatedly until stable amplitudes were reached and the electroretinogram was recorded at five minute intervals. Hypoxia was induced for 15, 30, and 45 minutes, after which the oxygen saturation was restored. The extent of the cell damage and glial reactivity was determined by Ethidium homodimer-1 staining, immunohistochemistry, and Western blot. biResults/i/bbi /i/bHypoxia caused a time-dependent reduction of the b-wave amplitudes, which could not be prevented by the H-1152P. Although the Rho-kinase inhibitor maintained higher b-wave amplitudes, these effects did not reach statistical significance. Hypoxia also resulted in an increase in cell damage and the activation of the glial cells in the untreated retinas whereas the administration of H-1152P significantly reduced the extent of these events. biConclusion /i/bH-1152P exerted a neuroprotective effect against necrosis on the isolated bovine retina under hypoxia together with a reduction in glial cell reactivity. However, the inhibitor could not prevent the hypoxia induced retinal dysfunction possibly due to the interference with synaptic modulation.
机译：目标 研究缺氧条件下分离的灌注脊椎动物视网膜电生理学模型中Rho激酶抑制的结果。 方法 用或不使用Rho激酶抑制剂H-1152P的氧饱和营养液灌注牛视网膜。重复刺激视网膜直至达到稳定的振幅，并以五分钟的间隔记录视网膜电图。缺氧持续15分钟，30分钟和45分钟，然后恢复氧饱和度。通过Ethidium homodimer-1染色，免疫组化和Western印迹确定细胞损伤的程度和神经胶质反应性。 结果 缺氧导致b波振幅随时间的减小，这是无法避免的。 H-1152P。尽管Rho激酶抑制剂维持较高的b波振幅，但这些影响并未达到统计学意义。缺氧还导致未经处理的视网膜中细胞损伤的增加和神经胶质细胞的活化，而H-1152P的给药显着降低了这些事件的程度。 结论 H-1152P在缺氧条件下对离体的牛视网膜具有抗坏死的神经保护作用，并且胶质细胞反应性降低。但是，该抑制剂可能不能预防由缺氧引起的视网膜功能障碍，这可能是由于对突触调节的干扰。

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