The mitochondrial and endoplasmic reticulum pathways involved in the apoptosis of bursa of Fabricius cells in broilers exposed to dietary aflatoxin B1
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Shibin Yuan1,2,*, Bangyuan Wu1,2,*, Zhengqiang Yu3,*, Jing Fang3, Na Liang3, Mingqiang Zhou1,2, Cheng Huang1,2, Xi Peng1,2
1Department of Wild Animal Disease, College of Life Science, China West Normal University, Nanchong 637009, Sichuan, The People’s Republic of China
2Key Laboratory of Southwest China Wildlife Resources Conservation (China West Normal University), Ministry of Education, Nanchong 637009, Sichuan, The People’s Republic of China
3Department of Animal Pathlogy, College of Veterinary Medicine, Sichuan Agricultural University, Ya’an 625014, Sichuan, The People’s Republic of China
*These authors have contributed equally to this work
Xi Peng, email: email@example.com
Keywords: aflatoxin B1, bursa of Fabricius, apoptosis, oxidative stress, broiler
Received: May 27, 2016 Accepted: July 28, 2016 Published: August 17, 2016
Aflatoxin B1 (AFB1), a toxic metabolite produced by some fungi, exerts well-known hepatocarcinogenic and immunosuppressive effects, the latter can increase the apoptotic immune cells in vitro. However, it is largely unknown that which signaling pathways contribute to excessive apoptosis of immune cells which induced by AFB1. In this study, we investigated the roles of the mitochondria, endoplasmic reticulum (ER) and death receptor activated apoptotic pathways in the bursal of Fabricius (BF) cells in the broilers exposed to AFB1 diet. We found that (1) AFB1 diet induced morphological changes in the BF. (2) FCM and TUNEL methods showed that excessive apoptosis could be resulted from AFB1 intake. (3) AFB1-induced apoptosis of bursal cells involved mitochondrial pathway (increase of Bax, Bak, cytC, caspase-9, Apaf-1, caspase-3 and decrease of Bcl-2 and Bcl-xL) and ER pathway (increase of Grp78/Bip, Grp94 and CaM). (4) Oxidative stress was confirmed in the BF of chicken fed on AFB1 diet. Overall, this work is the first to demonstrate that the activation of mitochondria and ER apoptosis pathways can lead to excessive apoptosis in BF cells, and oxidative stress is a crucial driver during AFB1 exposure.
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