Bovine lactoferrin alleviates aflatoxin B1 induced hepatic and renal injury in broilers by mediating Nrf2 signaling pathway.

Autor:	Chen H; Department of Basic Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi Province, 712100, China., Buzdar JA; Department of Basic Veterinary Science, Faculty of Veterinary & Animal Science, Lasbela University of Agriculture, Water and Marine Sciences, Uthal, 90150, Baluchistan, Pakistan., Riaz R; Department of Animal Nutrition and Nutritional Diseases, Faculty of Veterinary Medicine, Kafkas University, Kars, 36100, Türkiye., Fouad D; Zoology Department, College of Science, King Saud University, 11451, Riyadh, Saudi Arabia., Ahmed N; Department of Basic Veterinary Science, Faculty of Veterinary & Animal Science, Lasbela University of Agriculture, Water and Marine Sciences, Uthal, 90150, Baluchistan, Pakistan., Shah QA; Department of Basic Veterinary Science, Faculty of Veterinary & Animal Science, Lasbela University of Agriculture, Water and Marine Sciences, Uthal, 90150, Baluchistan, Pakistan., Chen S; Department of Basic Veterinary Medicine, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi Province, 712100, China. Electronic address: csl_1359@163.com.
Jazyk:	angličtina
Zdroj:	Poultry science [Poult Sci] 2024 Sep 19; Vol. 103 (12), pp. 104316. Date of Electronic Publication: 2024 Sep 19.
DOI:	10.1016/j.psj.2024.104316
Abstrakt:	Aflatoxin B1 (AFB1) a mycotoxin found in chicken feed that possess a global hazard to poultry health. However different potent compounds like bovine lactoferrin (bLF) may prove to be protective effects against AFB1. This study aims to explore the protective effect of bLF against AFB1-induced injury in the liver and kidney in broiler. For this purpose, 600 broilers chicks were randomly alienated into 5 groups (n = 120 each): negative control; positive control (3 mg/kg AFB1), and bLF high, medium, and low dosage groups (600 mg/kg, 300 mg/kg, and 150 mg/kg, respectively). The results highlight that AFB1 toxicity in birds exhibited low feed intake, reduction in weight gain, and a decrease in FCR while, bLF regulated these adverse effects. Meanwhile, AFB1 group showed higher levels of alanine transaminase (ALT) and aspartate aminotransferase (AST) and lower levels of superoxide dismutase (SOD) and glutathione (GSHpx) in liver, while urea and creatinine were decline in kidney. Supplementation with bLF effectively controlled these biomarkers and control the negative effects of toxicity. Furthermore, hematoxylin and eosin (H&E) staining exhibited normal morphological structures within liver and kidney in the bLF treated groups, while degenerative changes were observed in AFB1 group. Similarly, bLF, decreased oxidative stress and thus prevented apoptosis in the liver and kidney cells of the birds. Whereas, mRNA level of mitochondrial apoptosis related gene including Bcl-2 (Bak and Bax), caspase-3 and caspase-9 was upregulated, while bcl2 gene were downregulated in AFB1 group. Dietary supplementation of bLF effectively normalizes the expression of these genes. AFB1 exposed birds shown to decrease gene expression level of the crucial component of Nrf2 pathway, responsible to regulate antioxidant defense. Interestingly, bLF reverse these detrimental effects of and restore the normal expression levels of Nrf2 pathway. Conclusively, our findings demonstrate that bLF mitigates the detrimental effects of AFB1, besides regulation of the apoptosis-related genes via mitochondrial pathways. These findings validate that the bLF (600 mg/kg) could be used as protective agent against AFB1-induced liver and kidney damage. Competing Interests: DISCLOSURES No conflict of interest exists in the submission of this manuscript, and the manuscript is approved by all authors for publication. I would like to declare on behalf of my co-authors that the work described was original research that has not been published previously, and not under consideration for publication elsewhere, in whole or in part. All the authors listed have approved the manuscript that is enclosed. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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