绿茶多酚(-)-表没食子儿茶素-3-没食子酸酯防止紫外线诱导的PC12细胞凋亡

S. Woo, Kim Yoon-Jung, Bangrong Cai, S. Park, Young Ho Kim, Ok-Joon Kim, I. Kang, Won-Jae Kim, Ji-Yeon Jung
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摘要

绿茶多酚(-)-表没食子儿茶素-3-没食子酸酯(EGCG)是一种有效的抗氧化剂,对神经毒性具有保护作用。然而,目前还不清楚EGCG是否能保护神经细胞免受辐射引起的损伤。因此,本研究旨在探讨EGCG对紫外线(UV)诱导的PC12细胞氧化应激和凋亡的影响。紫外线照射的影响包括细胞凋亡,这与DNA断裂、活性氧(ROS)的产生、caspase-3和caspase-9活性的增强以及聚(adp -核糖)聚合酶的裂解有关。紫外线照射也增加了Bax/Bcl-2比值和线粒体途径相关的细胞色素c表达。然而,在紫外线照射前用EGCG预处理可显著降低紫外线诱导的DNA断裂和ROS的产生。此外,紫外线照射诱导的Bax/Bcl-2比值升高、细胞色素c上调、caspase-3和caspase-9活化均可通过EGCG预处理得到改善。此外,EGCG抑制了紫外线诱导的p38磷酸化,并挽救了紫外线下调的ERK磷酸化。综上所述,这些结果表明EGCG通过清除活性氧和抑制已知在凋亡中起关键作用的线粒体途径来阻止紫外线照射诱导的PC12细胞凋亡。此外,EGCG通过JNK失活和ERK活化抑制uv诱导的PC12细胞凋亡。因此,EGCG是一种潜在的神经保护剂,可用于预防紫外线照射诱导的神经元细胞死亡。
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Green tea polyphenol (–)-epigallocatechin-3-gallate prevents ultraviolet-induced apoptosis in PC12 cells
Green tea polyphenol (–)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiationinduced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiationinduced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.
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