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Isolation of Bacillus licheniformis and its protective effect on liver oxidative stress and apoptosis induced by aflatoxin B1

文献类型： 外文期刊

作者： Dong, Wenwen 1 ; Liu, Mingchao 2 ; Liu, Bei 1 ; Xiao, Yaqing 1 ; Liu, Xia 1 ; Yang, Menghao 1 ; Yuan, Xiaoyuan 1 ; Li, Guiming 1 ; Meng, Kai 1 ;

作者机构： 1.Shandong Acad Agr Sci, Poultry Inst, Poultry Breeding Engn Technol Ctr Shandong Prov, Shandong Prov Key Lab Poultry Dis Diag & Immunol,J, Jinan 250023, Peoples R China

2.Hebei Agr Univ, Coll Vet Med, Baoding 071001, Peoples R China

3.Shandong Agr Univ, Res Ctr Anim Dis Control Engn, Tai An 271018, Shandong, Peoples R China

关键词： aflatoxin B1; Bacillus licheniformis; liver oxidative stress; apoptosis

期刊名称：POULTRY SCIENCE （ 影响因子：3.8； 五年影响因子：4.1 ）

ISSN： 0032-5791

年卷期： 2024 年 103 卷 10 期

页码：

收录情况： SCI

摘要： Aflatoxin B1 (AFB1) is one of the most toxic mycotoxins. The use of probiotics is an effective approach to reduce aflatoxins content in foods. To find efficient bacterial species that can eliminate or detoxify AFB1, a bacterial strain S51 capable of degrading AFB1 was isolated from chicken intestine and soil samples by using a culture medium containing coumarin as the sole carbon source. Based on the results of 16S rRNA gene sequence analysis, this isolate (strain S51) was identified as Bacillus licheniformis strain QT338. Further characterization of strain S51 showed that it could degrade AFB1 by 61.3% after incubation at 30 degrees C for 72 h. Additional studies demonstrated that S51 promoted good growth performance of the treated chickens, showed no hemolytic activity, carried few drug resistance genes, and exhibited a certain level of tolerance to acid and bile salts. Furthermore, to verify whether strain S51 exerts a protective effect on AFB1-induced liver injury in chickens and to elucidate the underlying mechanism, a chicken toxicity model was induced with AFB1 (100 mg/kg BW) and treated with S51(1x10(9)CFU/mL) for 12 d. The results showed that S51 decreased the level of alanine transaminase, aspartate transaminase, and total bilirubin (P P < 0.05); increased glutathione activity and total antioxidant capacityin the liver induced by AFB1, and decreased malondialdehyde production (P < 0.05). S51 also up-regulated the mRNA expression level of the antioxidant proteins HO-1 and Nrf2 and down-regulated the expression of the oxidation-related factor Keap1 in the Nrf2/Keap1 signaling pathway (P <0.05). S51 inhibited hepatocyte apoptosis induced by AFB1 and decreased the mRNA expression levels of the apoptosis-related genes Bax, caspase-3, caspase-9, and Cyt-C ( P < 0.05). These results indicate that S51 regulates apoptosis and alleviates AFB1-induced oxidative stress in chicken liver by controlling the Nrf2/Keap1 signaling pathway.

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