绿茶提取物可改善大鼠缺血性视网膜神经节细胞变性。
Green Tea Extract Ameliorates Ischemia-Induced Retinal Ganglion Cell Degeneration in Rats.
机构信息
Department of Ophthalmology and Vision Science, Eye and Ear Nose Throat Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Joint Shantou International Eye Center of Shantou University and the Chinese University of Hong Kong, Shantou, Guangdong, China.
出版信息
Oxid Med Cell Longev. 2019 Jul 9;2019:8407206. doi: 10.1155/2019/8407206. eCollection 2019.
PURPOSE
Oxidative stress induced by reduced blood circulation is a critical pathological damage to retinal ganglion cells (RGCs) in glaucoma. We previously showed that green tea extract (GTE) and its catechin constituents alleviate sodium iodate-induced retinal degeneration in rats. Here, we investigated the therapeutic effect of GTE on ischemia-induced RGC degeneration in rats.
METHODS
RGC degeneration was induced by ischemic reperfusion in adult Fischer F344 rats. Green tea extract (Theaphenon E) was intragastrically administered 4 times within 48 hours after ischemia. RGC survival, pupillary light reflex, expressions of cell apoptosis, oxidative stress, and inflammation-related proteins were studied.
RESULTS
Ischemic reperfusion significantly induced apoptotic RGCs, RGC loss, and larger constricted pupil area compared to the untreated normal rats. Expressions of activated caspase-3 and caspase-8, Sod2, and inflammation-related proteins as well as p38 phosphorylation were significantly upregulated in the ischemia-injured rats. Compared to the saline-fed ischemic rats, significantly higher number of surviving RGCs, less apoptotic RGCs, and smaller constricted pupil area were observed in the GTE-fed ischemic rats. GTE also reduced the increased protein expressions caused by ischemic injury but enhanced the Jak phosphorylation in the retina. Notably, green tea extract did not affect the survival of RGCs in the uninjured normal rats.
CONCLUSIONS
In summary, GTE offers neuroprotection to RGCs under ischemic challenge, suggesting a potential therapeutic strategy for glaucoma and optic neuropathies.
目的
由血液循环减少引起的氧化应激是青光眼中原发性节细胞（RGC）损伤的关键病理机制。我们之前已经证明，绿茶提取物（GTE）及其儿茶素成分可减轻碘酸钠诱导的大鼠视网膜变性。在此，我们研究了 GTE 对大鼠缺血诱导的 RGC 变性的治疗作用。
方法
通过成年 Fischer F344 大鼠的缺血再灌注诱导 RGC 变性。GTE（Theaphenon E）在缺血后 48 小时内通过胃内给药 4 次。研究了 RGC 存活、瞳孔光反射、细胞凋亡、氧化应激和炎症相关蛋白的表达。
结果
与未处理的正常大鼠相比，缺血再灌注显著诱导了凋亡的 RGC、RGC 丢失和更大的瞳孔收缩面积。与盐水喂养的缺血大鼠相比，缺血损伤大鼠中激活的 caspase-3 和 caspase-8、Sod2 和炎症相关蛋白的表达以及 p38 磷酸化明显上调。与缺血性损伤的盐水喂养大鼠相比，GTE 喂养的缺血大鼠中存活的 RGC 数量更高，凋亡的 RGC 数量更少，瞳孔收缩面积更小。GTE 还降低了缺血损伤引起的蛋白表达增加，但增强了视网膜中的 Jak 磷酸化。值得注意的是，绿茶提取物对未受损的正常大鼠中 RGC 的存活没有影响。
结论
总之，GTE 为缺血应激下的 RGC 提供了神经保护作用，为青光眼和视神经病变提供了一种潜在的治疗策略。
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