Epigallocatechin-3-gallate opposes HBV-induced incomplete autophagy by enhancing lysosomal acidification, which is unfavorable for HBV replication.
Epigallocatechin-3-gallate opposes HBV-induced incomplete autophagy by enhancing lysosomal acidification, which is unfavorable for HBV replication.
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DOI：
10.1038/cddis.2015.136
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发表时间：
2015-05-21
影响因子：
9
通讯作者：
Xiong S
中科院分区：
文献类型：
--
作者：
Zhong L;Hu J;Shu W;Gao B;Xiong S
表没食子儿茶素-3-没食子酸酯 (EGCG) 是绿茶中的一种主要多酚，具有多种有益特性，包括抗病毒活性。自噬是一种细胞过程，涉及长寿蛋白质和受损细胞器的降解。最近的证据表明，自噬的调节是多种病毒性疾病的潜在治疗策略。在本研究中，我们研究了 EGCG 对乙型肝炎病毒 (HBV) 复制的影响以及自噬在此过程中可能的参与。我们的结果表明，HBV 诱导自噬体形成，这是自身复制所必需的。然而，虽然 EGCG 有效抑制 HBV 复制，但它增强但不抑制肝癌细胞中自噬体的形成。进一步研究表明，HBV诱导不完全自噬，而EGCG与饥饿类似，能够诱导完全自噬过程，这似乎不利于HBV复制。此外，研究发现，HBV 通过损害溶酶体酸化诱导不完全自噬，而在 EGCG 存在下则失去了这种能力。综上所述，这些数据表明，EGCG 治疗通过增强溶酶体酸化来对抗 HBV 诱导的不完全自噬，这不利于 HBV 复制。
Epigallocatechin-3-gallate (EGCG), a major polyphenol in green tea, exhibits diverse beneficial properties, including antiviral activity. Autophagy is a cellular process that is involved in the degradation of long-lived proteins and damaged organelles. Recent evidence indicates that modulation of autophagy is a potential therapeutic strategy for various viral diseases. In the present study, we investigated the effect of EGCG on hepatitis B virus (HBV) replication and the possible involvement of autophagy in this process. Our results showed that HBV induced autophagosome formation, which was required for replication of itself. However, although EGCG efficiently inhibited HBV replication, it enhanced, but not inhibited, autophagosome formation in hepatoma cells. Further study showed that HBV induced an incomplete autophagy, while EGCG, similar to starvation, was able to induce a complete autophagic process, which appeared to be unfavorable for HBV replication. Furthermore, it was found that HBV induced an incomplete autophagy by impairing lysosomal acidification, while it lost this ability in the presence of EGCG. Taken together, these data demonstrated that EGCG treatment opposed HBV-induced incomplete autophagy via enhancing lysosomal acidification, which was unfavorable for HBV replication.