Lv Hongli, Wang Jingjing, Geng Yuan, Xu Tianchao, Han Fuxin, Gao Xue-Jiao, Guo Meng-Yao
College of Veterinary Medicine, Northeast Agricultural University, Harbin, China.
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Food Funct. 2024 Apr 2;15(7):3411-3419. doi: 10.1039/d4fo00480a.
Tetrabromobisphenol A (TBBPA) is a global pollutant. When TBBPA is absorbed by the body through various routes, it can have a wide range of harmful effects on the body. Green tea polyphenols (GTPs) can act as antioxidants, resisting the toxic effects of TBBPA on animals. The effects and mechanisms of GTP and TBBPA on oxidative stress, inflammation and apoptosis in the mouse lung are unknown. Therefore, we established and models of TBBPA exposure and GTP antagonism using C57 mice and A549 cells and examined the expression of factors related to oxidative stress, autophagy, inflammation and apoptosis. The results of the study showed that the increase in reactive oxygen species (ROS) levels after TBBPA exposure decreased the expression of autophagy-related factors Beclin1, LC3-II, ATG3, ATG5, ATG7 and ATG12 and increased the expression of p62; oxidative stress inhibits autophagy levels. The increased expression of the pro-inflammatory factors IL-1β, IL-6 and TNF-α decreased the expression of the anti-inflammatory factor IL-10 and activation of the NF-κB p65/TNF-α pathway. The increased expression of Bax, caspase-3, caspase-7 and caspase-9 and the decreased expression of Bcl-2 activate apoptosis-related pathways. The addition of GTP attenuated oxidative stress levels, restored autophagy inhibition and reduced the inflammation and apoptosis levels. Our results suggest that GTP can attenuate the toxic effects of TBBPA by modulating ROS, reducing oxidative stress levels, increasing autophagy and attenuating inflammation and apoptosis in mouse lung and A549 cells. These results provide fundamental information for exploring the antioxidant mechanism of GTP and further for studying the toxic effects of TBBPA.
四溴双酚A（TBBPA）是一种全球污染物。当TBBPA通过各种途径被人体吸收时，它会对人体产生广泛的有害影响。绿茶多酚（GTPs）可以作为抗氧化剂，抵抗TBBPA对动物的毒性作用。GTP和TBBPA对小鼠肺组织氧化应激、炎症和凋亡的影响及机制尚不清楚。因此，我们利用C57小鼠和A549细胞建立了TBBPA暴露和GTP拮抗模型，并检测了氧化应激、自噬、炎症和凋亡相关因子的表达。研究结果表明，TBBPA暴露后活性氧（ROS）水平升高，降低了自噬相关因子Beclin1、LC3-II、ATG3、ATG5、ATG7和ATG12的表达，增加了p62的表达；氧化应激抑制自噬水平。促炎因子IL-1β、IL-6和TNF-α表达增加，降低了抗炎因子IL-10的表达，并激活了NF-κB p65/TNF-α信号通路。Bax、caspase-3、caspase-7和caspase-9表达增加，Bcl-2表达降低，激活了凋亡相关信号通路。添加GTP可降低氧化应激水平，恢复自噬抑制，并降低炎症和凋亡水平。我们的结果表明，GTP可以通过调节ROS、降低氧化应激水平、增加自噬以及减轻小鼠肺组织和A549细胞的炎症和凋亡来减轻TBBPA的毒性作用。这些结果为探索GTP的抗氧化机制以及进一步研究TBBPA的毒性作用提供了基础信息。
