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首页> 外文期刊>Biochemical and Biophysical Research Communications >Epigallocatechin-gallate (EGCG) regulates autophagy in human retinal pigment epithelial cells: A potential role for reducing UVB light-induced retinal damage
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Epigallocatechin-gallate (EGCG) regulates autophagy in human retinal pigment epithelial cells: A potential role for reducing UVB light-induced retinal damage

机译：Epigallocatechin-gallate（EGCG）调节人视网膜色素上皮细胞的自噬：减少UVB光诱导的视网膜损伤的潜在作用

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摘要

Autophagy is an intracellular catabolic process involved in protein and organelle degradation via the lysosomal pathway that has been linked in the pathogenesis of age-related macular degeneration (AMD). UVB irradiation-mediated degeneration of the macular retinal pigment epithelial (RPE) cells is an important hallmark of AMD, which is along with the change in RPE autophagy. Thus, pharmacological manipulation of RPE autophagy may offer an alternative therapeutic target in AMD. Here, we found that epigallocatechin-3-gallate (EGCG), a polyphenolic compound from green tea, plays a regulatory role in UVB irradiation-induced autophagy in RPE cells. UVB irradiation results in a marked increase in the amount of LC3-II protein in a dose-dependent manner. EGCG administration leads to a significant reduction in the formation of LC3-II and autophagosomes. mTOR signaling activation is required for EGCG-induced LC3-II formation, as evidenced by the fact that EGCG-induced LC3-II formation is significantly impaired by rapamycin administration. Moreover, EGCG significantly alleviates the toxic effects of UVB irradiation on RPE cells in an autophagy-dependent manner. Collectively, our study reveals a novel role of EGCG in RPE autophagy. EGCG may be exploited as a potential therapeutic reagent for the treatment of pathological conditions associated with abnormal autophagy.
机译：自噬是一种细胞内分解代谢过程，通过溶酶体途径参与蛋白质和细胞器的降解，该途径与年龄相关性黄斑变性（AMD）的发病机理有关。 UVB辐射介导的黄斑视网膜色素上皮细胞（RPE）变性是AMD的重要标志，它与RPE自噬的变化一起。因此，RPE自噬的药理学操纵可为AMD提供替代治疗靶点。在这里，我们发现Epigallocatechin-3-gallate（EGCG），一种来自绿茶的多酚化合物，在UVB辐射诱导的RPE细胞自噬中起调节作用。 UVB辐射以剂量依赖性方式导致LC3-II蛋白的量显着增加。 EGCG施用导致LC3-II和自噬小体形成的显着减少。 EGCG诱导的LC3-II形成需要mTOR信号激活，这一事实证明，雷帕霉素的给药显着损害了EGCG诱导的LC3-II形成。此外，EGCG以自噬依赖性方式显着减轻了UVB辐射对RPE细胞的毒性作用。总的来说，我们的研究揭示了EGCG在RPE自噬中的新作用。 EGCG可被用作治疗与异常自噬相关的病理状况的潜在治疗剂。

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