Abstract

With the promotion of the intensive breeding model, the incidence of leg diseases has risen in fast-growing commercial broilers with higher body weight, seriously affecting their feed efficiency and causing animal welfare problems. Femoral head necrosis (FHN) is the most common leg disease in broilers. Previous studies reported that hormone-induced FHN is related to endoplasmic reticulum (ER) stress, apoptosis, and oxidative stress, but no detailed study has been conducted in broilers with spontaneous FHN. In the study, the articular cartilage of 5-wk-old Ross 308 broilers with spontaneous FHN was used to investigate the pathogenesis of the disease. According to the degree of femoral head injury, the birds participating in the experiment were divided into 3 groups, namely a control group, femoral head separation group and femoral head separation with growth plate lacerations group. The morphological changes in articular cartilage were observed by hematoxylin and eosin, toluidine blue, alcian blue and safranine O-solid green staining, and the expressions of genes related to cartilage homeostasis, ER stress, autophagy, apoptosis and oxidative stress was detected using Real-Time Quantitative PCR. In the results, the expression of aggrecan and collagen-2 mRNA levels decreased in the articular cartilage of spontaneous FHN broilers, and the same changes were observed in the tissue staining results, indicating the disordered nature of articular cartilage homeostasis. At the same time, FHN in broilers causes ER stress in articular chondrocytes and regulates oxidative stress by activating the nuclear factor erythroid 2-related factor 2/antioxidant response element pathway through protein kinase RNA-like ER kinase. Autophagy can be activated through the protein kinase RNA-like ER kinase-activating transcription factor-4 pathway, and apoptosis can even be activated through CCAAT-enhancer-binding protein homologous protein. Therefore, the secretory activity of articular chondrocytes in spontaneous FHN broilers is negatively affected, which leads to the disorder of cartilage homeostasis and results in FHN due to ER-stress-mediated chondrocyte apoptosis and oxidative stress.

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