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黄曲霉毒素B1诱导空肠G2M细胞周期阻滞的分子机制。

The molecular mechanism of G2M cell cycle arrest induced by AFB1 in the jejunum.

作者信息

Yin Heng, Jiang Min, Peng Xi, Cui Hengmin, Zhou Yi, He Min, Zuo Zhicai, Ouyang Ping, Fan Junde, Fang Jing

机构信息

Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Chengdu, Sichuan, PR China.

College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan, PR China.

出版信息

Oncotarget. 2016 Jun 14;7(24):35592-35606. doi: 10.18632/oncotarget.9594.

Abstract

Aflatoxin B1 (AFB1) has potent hepatotoxic, carcinogenic, genotoxic, immunotoxic and other adverse effects in human and animals. The aim of this study was to investigate the molecular mechanism of G2/M cell cycle arrest induced by AFB1 in the jejunum of broilers. Broilers, as experimental animals, were fed 0.6 mg/kg AFB1 diet for 3 weeks. Our results showed that AFB1 reduced the jejunal villus height, villus height/crypt ratio and caused G2/M cell cycle arrest. The G2/M cell cycle was accompanied by the increase of ataxia telangiectasia mutated (ATM), p53, Chk2, p21 protein and mRNA expression, and the decrease of Mdm2, cdc25C, cdc2, cyclin B and proliferating cell nuclear antigen protein and mRNA expression. In conclusion, AFB1 blocked G2/M cell cycle by ATM pathway in the jejunum of broilers.

摘要

黄曲霉毒素B1(AFB1)对人和动物具有强大的肝毒性、致癌性、遗传毒性、免疫毒性及其他不良反应。本研究旨在探讨AFB1诱导肉鸡空肠G2/M期细胞周期阻滞的分子机制。以肉鸡作为实验动物,用含0.6 mg/kg AFB1的饲料喂养3周。我们的结果表明,AFB1降低了空肠绒毛高度、绒毛高度/隐窝比值,并导致G2/M期细胞周期阻滞。G2/M期细胞周期伴随着共济失调毛细血管扩张症突变基因(ATM)、p53、Chk2、p21蛋白及mRNA表达的增加,以及Mdm2、cdc25C、cdc2、细胞周期蛋白B和增殖细胞核抗原蛋白及mRNA表达的减少。综上所述,AFB1通过ATM途径阻滞了肉鸡空肠的G2/M期细胞周期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b125/5094947/70bf2613d0ec/oncotarget-07-35592-g001.jpg

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