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TBBPA caused multiple intestinal injuries via ROS/NF-κB signal in common carp
Aquatic Toxicology ( IF 4.1 ) Pub Date : 2024-12-01 , DOI: 10.1016/j.aquatox.2024.107190
Man Qian, Yuan Geng, Jing-jing Wang, Hong-ru Wang, Ji-long Luo, Xue-jiao Gao

Tetrabromobisphenol A (TBBPA) is an aquatic environment's prevalent pollutant, posing a great threat to the health of aquatic animals. The intestine is a key organ for nutrient absorption as well as an important barrier to prevent pollutants from invading the body of fish. Exploring the effects of pollutants on the intestine is of great significance for maintaining fish health. Therefore, the purpose of this study was to assess the toxic effects of TBBPA on the intestine of Cyprinus carpio L. (common carp) by establishing models of common carp and primary intestinal epithelial cells exposed to TBBPA. Histological observation revealed that TBBPA exposure led to damage in the intestinal mucosa and breakage of intestinal villi. Detection of oxidative stress levels showed that TBBPA increased the levels of ROS and MDA, and decreased the activity of SOD, CAT, GSH-PX, and T-AOC in intestinal tissue and cells. Observation of inflammatory factor levels revealed that TBBPA upregulated the mRNA levels of inflammatory factors (IL-6, TNF-α, IL-1β, NF-κB p65 and IκBα). ELISA and western blotting results were consistent with the mRNA results. Moreover, TBBPA induced cell death, as evidenced by TUNEL staining and flow cytometry and confirmed by increasing levels of Bax, Cas-3, Cyt C, RIP1, RIP3, and MLKL, together with decreasing the levels of Bcl-2. TBBPA also destroyed the intestinal tight junction by reducing the mRNA and protein levels of claudin-1, ZO-1, and occludin. In summary, this study reveals that TBBPA caused intestinal injuries, inducing oxidative stress, inflammation, cell death, and tight junction disruption via ROS/NF-κB signal in common carp.

中文翻译:


TBBPA 通过 ROS/NF-κB 信号在鲤鱼中引起多发性肠道损伤



四溴双酚 A (TBBPA) 是水生环境中普遍存在的污染物,对水生动物的健康构成巨大威胁。肠道是营养吸收的关键器官,也是防止污染物侵入鱼体的重要屏障。探索污染物对肠道的影响对于维持鱼类健康具有重要意义。因此,本研究的目的是通过建立暴露于 TBBPA 的鲤鱼和原代肠上皮细胞的模型来评估 TBBPA 对鲤鱼肠道的毒性作用。组织学观察显示,TBBPA 暴露导致肠粘膜损伤和肠绒毛破裂。氧化应激水平检测显示,TBBPA 增加肠道组织和细胞中 ROS 和 MDA 的水平,降低 SOD、CAT、GSH-PX 和 T-AOC 的活性。炎症因子水平的观察显示,TBBPA 上调了炎症因子 (IL-6 、 TNF-α 、 IL-1β 、 NF-κB p65 和 IκBα 的 mRNA 水平。ELISA 和 western blotting 结果与 mRNA 结果一致。此外,TBBPA 诱导细胞死亡,TUNEL 染色和流式细胞术证明了这一点,并通过 Bax、Cas-3、Cyt C、RIP1、RIP3 和 MLKL 水平升高以及 Bcl-2 水平降低来证实。TBBPA 还通过降低 claudin-1、ZO-1 和 occludin 的 mRNA 和蛋白质水平来破坏肠道紧密连接。综上所述,本研究揭示了 TBBPA 通过鲤鱼的 ROS/NF-κB 信号引起肠道损伤,诱导氧化应激、炎症、细胞死亡和紧密连接破坏。
更新日期:2024-12-01
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