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槲皮素通过ROS/MAPK/NF-κB途径减轻邻苯二甲酸二(2-乙基己基)酯暴露引发的雏鸡法氏囊细胞焦亡和坏死性凋亡。

Quercetin Alleviates Pyroptosis and Necroptosis Triggered on by DEHP Exposure in Bursa of Fabricius in Chicken by the ROS/MAPK/NF-κB Pathway.

作者信息

Huang Chenxi, Wang Xiaodan, Zhang Wenwen, Liu Meichen, Xie Ruirui, Zheng Huiling, Huo Xinyu, Xu Tong, Lin Hongjin

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China.

Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, P. R. China.

出版信息

J Agric Food Chem. 2025 Apr 16;73(15):9337-9347. doi: 10.1021/acs.jafc.5c00224. Epub 2025 Apr 2.

Abstract

Bis(2-ethylhexyl) phthalate (DEHP) is an endocrine disruptor that may cause damage to several species. Quercetin (Que), a common flavonoid, has anti-inflammation, antioxidation, and immune regulation properties. In this study, we identified DEHP-exposed or Que-antagonist groups in chicken and MSB-1 cells to explore whether Que can mitigate DEHP-caused bursa of Fabricius pyroptosis and necroptosis. The findings demonstrated that Que reduced the expression of necroptosis and pyroptosis, inhibited the mitogen-activated protein kinase (MAPK)/NF-κB pathway, and mitigated oxidative stress caused by DEHP. The addition of the reactive oxygen species activator (Sanguinarin) raised the extent of oxidative stress, and the NF-κB activator (nuclear factor-kappa-B activator1, NF-κB act1) activated the MAPK/NF-κB pathway compared to the Que + DEHP group. In conclusion, Que inhibited the MAPK/NF-κB pathway to counteract DEHP-induced bursa pyroptosis and programmed necrosis. This work adds to the toxicological consequences of DEHP on avian further theoretical justification for Que's treatment of organic toxic damage.

摘要

邻苯二甲酸二(2-乙基己基)酯(DEHP)是一种内分泌干扰物,可能会对多种物种造成损害。槲皮素(Que)是一种常见的黄酮类化合物,具有抗炎、抗氧化和免疫调节特性。在本研究中,我们在鸡和MSB-1细胞中确定了DEHP暴露组或Que拮抗剂组,以探讨Que是否可以减轻DEHP引起的法氏囊细胞焦亡和坏死性凋亡。研究结果表明,Que降低了坏死性凋亡和细胞焦亡的表达,抑制了丝裂原活化蛋白激酶(MAPK)/核因子κB(NF-κB)信号通路,并减轻了DEHP引起的氧化应激。与Que + DEHP组相比,添加活性氧激活剂(血根碱)提高了氧化应激程度,NF-κB激活剂(核因子κB激活剂1,NF-κB act1)激活了MAPK/NF-κB信号通路。总之,Que通过抑制MAPK/NF-κB信号通路来对抗DEHP诱导的法氏囊细胞焦亡和程序性坏死。这项工作进一步补充了DEHP对禽类的毒理学后果,为Que治疗有机毒物损伤提供了理论依据。

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