ACTA VETERINARIA ET ZOOTECHNICA SINICA ›› 2017, Vol. 48 ›› Issue (9): 1744-1752.doi: 10.11843/j.issn.0366-6964.2017.09.021

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Study on Regulation Mechanism of Death Receptor Pathway Related to Up-regulated Apoptosis of Thymocytes in Broilers after AFB1 Exposure

PENG Xi1#*, LIANG Na2#, FANG Jing2*, WU Bang-yuan1   

  1. 1. College of Life Science, China West Normal University, Nanchong 637000, China;
    2. College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China
  • Received:2017-03-06 Online:2017-09-23 Published:2017-09-23

Abstract:

This experiment was conducted to investigate the regulation mechanism of death receptor pathway involved in the aflatoxins (AF) B1-induced thymocytes apoptosis. Ninety healthy chickens were randomly divided into two groups, and fed on control diet and AFB1 containing diet (formulated by adding 0.6 mg·kg-1 AFB1 into the control diet) respectively for 21 days. Thymus was sampled for detecting the relative weight, T-cell subsets, percentage of apoptotic cells and relative mRNA expression of genes in the death receptor pathway at 7, 14 and 21 days of age. Our results showed that in the AFB1 group, the relative weight of thymus was decreased; the percentages of CD3+, CD3+CD4+, CD3+CD8+ T-cells were decreased, and the percentage of apoptotic thymocytes was increased, when compared with those in the control group. Also, the relative mRNA transcription of RIP1, Caspase-8, Caspase-9, Caspase-3, Fas, FasL, ASK1, IKIP and JNK were up-regulated, and those of Bcl-2, NF-κB1 and Bid were down-regulated. It was speculated that the mechanisms of the excessive apoptosis of thymocytes could be related to the following three downstream death receptor pathways:①AFB1 could directly induce the apoptosis through the Fas-FasL-FADD-Caspase-8-Caspase-3 pathway; ②Fas could take part in the excessive apoptosis through Fas-ASK1-JNK-Bcl-2 pathway which was mediated via mitochondria; ③The constitutive activation of the TNF-α-RIP1-IKIP-NF-κB1-caspase-3 could be a pathway contributing to the apoptosis of thymocytes induced by AFB1.

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