Department of Ophthalmology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
Exp Eye Res. 2010 Apr;90(4):528-34. doi: 10.1016/j.exer.2010.01.007. Epub 2010 Jan 28.
The purpose of this study was to investigate the effects of epigallocatechin-3-gallate (EGCG) in axotomized eyes and the pathways related to its action. Wistar rats received intracranial optic nerve (ON) axotomy 2 mm behind the globe in left eyes, whereas right eyes received sham operations. EGCG was administrated via intraperitoneal injection 30 min before and 4 days after axotomy. The density of retinal ganglion cell (RGC) was examined by a retrograde labeling technique. Western blot analysis was used to assess the expression of neuronal nitric oxide synthase (nNOS), Bax, Bcl-2, ERK and Akt. Optic nerve axotomy caused 54% RGC loss 7 days following surgery, and EGCG treatment reduced RGC loss by 12% (P = 0.017). The expression of the nNOS and pro-apoptotic Bax proteins were increased 5 days after axotomy, while EGCG treatment significantly blunted the up-regulation of the above two proteins (P = 0.04 and 0.02, respectively). Axotomy-induced p-ERK 1/2 and p-Akt proteins expression 5 days and 3 days following injury, respectively. Treatment with EGCG further enhanced p-ERK 1/2 and p-Akt expressions after axotomy. Inhibition of ERK and Akt pathways attenuated the protection of EGCG on RGC against axotomy damage. Thus, we demonstrated that administration of EGCG prior to axotomy promotes RGC survival. The neuroprotective capacity of EGCG appears to act through mediating nitric oxide, anti-apoptotic, and cell survival signaling pathways.
本研究旨在探讨表没食子儿茶素没食子酸酯（EGCG）在视神经切断眼的作用及其相关途径。Wistar 大鼠左眼接受颅内视神经（ON） 2mm 后切断术，而右眼接受假手术。EGCG 在视神经切断前 30 分钟和切断后 4 天通过腹腔注射给药。通过逆行标记技术检查视网膜神经节细胞（RGC）的密度。Western blot 分析用于评估神经元型一氧化氮合酶（nNOS）、Bax、Bcl-2、ERK 和 Akt 的表达。视神经切断术后 7 天引起 54%的 RGC 丢失，而 EGCG 处理使 RGC 丢失减少 12%（P=0.017）。视神经切断后 5 天，nNOS 和促凋亡 Bax 蛋白的表达增加，而 EGCG 处理显著减弱了上述两种蛋白的上调（P=0.04 和 0.02）。视神经切断诱导的 p-ERK1/2 和 p-Akt 蛋白表达分别在损伤后 5 天和 3 天增加。EGCG 处理进一步增强了视神经切断后的 p-ERK1/2 和 p-Akt 表达。ERK 和 Akt 途径的抑制减弱了 EGCG 对 RGC 对抗视神经切断损伤的保护作用。因此，我们证明了视神经切断前给予 EGCG 可促进 RGC 存活。EGCG 的神经保护能力似乎通过介导一氧化氮、抗凋亡和细胞存活信号通路起作用。
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