Han Fuxin, Xu Ran, Wang Hongru, Gao Xuejiao, Guo Mengyao
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Animals (Basel). 2025 Aug 6;15(15):2307. doi: 10.3390/ani15152307.
Tetrabromobisphenol A (TBBPA), a widely utilised brominated flame retardant, demonstrates toxicological effects in aquatic organisms. Tea polyphenols (TPs), natural compounds found in tea leaves, exhibit both antioxidant and anti-inflammatory activities. The kidney is one of the major metabolic organs in common carp and serves as a target organ for toxic substances. This study evaluated the therapeutic potential of TPs in mitigating TBBPA-induced nephrotoxicity in common carp. Common carp were exposed to 0.5 mg/L TBBPA in water and/or fed a diet supplemented with 1 g/kg TPs for 14 days. In vitro, primary renal cells were treated with 60 μM TBBPA and/or 2.5 μg/L TPs for 24 h. Methods included histopathology, TUNEL assay for apoptosis, ROS detection, and molecular analyses. Antioxidant enzymes (SOD, CAT) and inflammatory cytokines (IL-1β, IL-6, TNF-α) were quantified using ELISA kits. Results showed that TBBPA induced oxidative stress, and activated the ROS-PI3K/AKT-NF-κB pathway, thereby resulting in inflammatory responses. TBBPA upregulated apoptosis-related genes (, , and ) and induced apoptosis. TBBPA upregulated the expression of RIPK3/MLKL, thereby exacerbating necroptosis. TPs intervention significantly mitigated these effects by reducing ROS, suppressing NF-κB activation, and restoring antioxidant enzyme activities (SOD, CAT). Moreover, TPs attenuated apoptosis and necrosis in the carp kidney, thereby enhancing the survival ability and immunity of common carp.
四溴双酚A（TBBPA）是一种广泛使用的溴化阻燃剂，对水生生物具有毒理学效应。茶多酚（TPs）是茶叶中含有的天然化合物，具有抗氧化和抗炎活性。肾脏是鲤鱼的主要代谢器官之一，也是有毒物质的靶器官。本研究评估了TPs对减轻鲤鱼TBBPA诱导的肾毒性的治疗潜力。将鲤鱼暴露于水中0.5 mg/L的TBBPA和/或喂食添加1 g/kg TPs的饲料14天。在体外，将原代肾细胞用60 μM TBBPA和/或2.5 μg/L TPs处理24小时。方法包括组织病理学、凋亡的TUNEL检测、ROS检测和分子分析。使用ELISA试剂盒对抗氧化酶（SOD、CAT）和炎性细胞因子（IL-1β、IL-6、TNF-α）进行定量。结果表明，TBBPA诱导氧化应激，并激活ROS-PI3K/AKT-NF-κB通路，从而导致炎症反应。TBBPA上调凋亡相关基因（、和）并诱导凋亡。TBBPA上调RIPK3/MLKL的表达，从而加剧坏死性凋亡。TPs干预通过降低ROS、抑制NF-κB激活和恢复抗氧化酶活性（SOD、CAT）显著减轻了这些影响。此外，TPs减轻了鲤鱼肾脏的凋亡和坏死，从而提高了鲤鱼的生存能力和免疫力。
