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首页> 外文期刊>Brain research >Epigallocatechin gallate, an active ingredient from green tea, attenuates damaging influences to the retina caused by ischemia/reperfusion.
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Epigallocatechin gallate, an active ingredient from green tea, attenuates damaging influences to the retina caused by ischemia/reperfusion.

机译：表没食子儿茶素没食子酸酯是绿茶的活性成分，可减轻缺血/再灌注对视网膜的破坏性影响。

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摘要

The aim of this study was to examine whether the antioxidant epigallocatechin gallate (EGCG), a catechin-base flavonoid derived from green tea protects retina neurones in situ from ischemia/reperfusion and in vitro from an oxidative stress insult of hydrogen peroxide (H(2)O(2)). Similar results were obtained when rats were injected by two different regimes of EGCG. Ischemia was delivered by raising the intraocular pressure above the systolic blood pressure (120 mm Hg) generally for 45 min. The electroretinogram (ERG) was measured prior to ischemia and 5 days after reperfusion. Rats were killed 7 days after ischemia and processed for immunohistochemistry and for determining of mRNA and protein levels by RT-PCR and electrophoresis/western blotting, respectively. In addition, optic nerves 7 days after ischemia were subjected to protein analysis. Ischemia/reperfusion caused a significant reduction in the a- and b-wave amplitudes of the ERGs, a decrease in retinal ganglion cell and photoreceptor specific proteins and mRNAs, an increase in retinal caspase-3 mRNA and protein, an increase in retinal caspase-8 mRNA, an increase in retinal GFAP protein and mRNA and a decrease in optic nerve proteins associated with ganglion cell axons. All these changes were significantly counteracted by EGCG. Moreover, EGCG clearly blunted ischemia/reperfusion-induced changes in the localisation of retinal Thy-1 and ChAT immunoreactivities. EGCG also significantly reduced the apoptosis to retinal ganglion cells (RGC-5 cells) in culture caused by H(2)O(2). The results of the study demonstrate that EGCG provides protection to retinal neurones from oxidative stress and ischemia/reperfusion.
机译：这项研究的目的是检查抗氧化剂表没食子儿茶素没食子酸酯（EGCG）是一种从绿茶中提取的儿茶素基类黄酮是否能保护视网膜神经元免于局部缺血/再灌注，并在体外免受过氧化氢（H（2 O（2））。当通过两种不同的EGCG方案给大鼠注射时，获得了相似的结果。通常通过将眼内压升高至收缩压（120 mm Hg）以上45分钟来递送缺血。在缺血前和再灌注后5天测量视网膜电图（ERG）。缺血7天后处死大鼠并进行免疫组织化学处理，并分别通过RT-PCR和电​​泳/ western印迹法测定mRNA和蛋白质水平。另外，对缺血7天后的视神经进行蛋白质分析。缺血/再灌注导致ERGs的a波和b波幅度显着降低，视网膜神经节细胞和感光细胞特异性蛋白和mRNA降低，视网膜caspase-3 mRNA和蛋白增加，视网膜caspase-增加8 mRNA，与神经节细胞轴突相关的视网膜GFAP蛋白和mRNA的增加以及视神经蛋白的减少。所有这些变化均被EGCG明显抵消。此外，EGCG明显减弱了缺血/再灌注引起的视网膜Thy-1定位和ChAT免疫反应性的变化。 EGCG还显着减少了由H（2）O（2）引起的培养物中视网膜神经节细胞（RGC-5细胞）的凋亡。研究结果表明，EGCG可保护视网膜神经元免受氧化应激和缺血/再灌注的侵害。

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