Abstract

Objectives: In this study, the influence of methylprednisolone (MP) and 3-methyladenine (3-MA) on chondrocyte autophagy and bone quality were determined to investigate the mechanisms of femoral head necrosis in broilers.Methods: Chickens were divided into four groups: control, MP, 3-MA, and 3-MA+MP groups. Blood and bone samples were collected for biochemistry assay and bone quality determination. Cartilage was separated from the femoral head for histopathological analysis and gene expression detection.Results: The results indicated that MP treatment significantly affected blood levels of alkaline phosphatase, high-density lipoprotein, calcium, phosphorus, bone alkaline phosphatase, and osteocalcin in broilers. Additionally, MP treatment significantly increased blood levels of cholesterol, low-density lipoprotein, triglyceride, carboxy-terminal telopeptide of type-I collagen, and tartrate-resistant acid phosphatase 5. MP treatment also significantly decreased the levels of bone parameters compared with these values in controls, inhibited the expression of collagen-2, aggrecan, and mammalian target of rapamycin, and increased the expression of beclin1 and microtubule-associated protein 1 light chain 3, hypoxia-inducible factor 1 alpha, phosphoinositide 3-kinase, protein kinase B and autophagy-related gene 5 of the femoral head. Furthermore, following co-treatment with 3-MA and MP, 3-MA mitigated the effects of MP.Conclusions: Our findings demonstrated that autophagy may be involved in the pathogenesis of femoral head necrosis induced by MP in broilers, and this study provides new treatment and prevention ideas for femoral head necrosis caused by glucocorticoids.

Highlights

  • The modern poultry industry focuses on selecting fast-growing broilers because of their short feeding period and high feed conversion ratio

  • MP treatment significantly increased the number of broilers which presented lameness (Gait score 3 and 4)

  • Broilers are suitable for use as experimental models of femoral head necrosis (FHN) induced by MP [13, 42]

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Summary

Introduction

The modern poultry industry focuses on selecting fast-growing broilers because of their short feeding period and high feed conversion ratio. GC treatment may increase the risk of fractures related to bone fragility and bone loss and cause femoral head necrosis (FHN) [2, 3]. Our previous study showed that chondrocyte apoptosis in the articular cartilage of the femoral head was an important characteristic of the pathological changes occurring in GC-induced broilers and related genes in endoplasmic reticulum stress (ERS) signaling pathway activated to promote apoptosis [13]. Previous studies reported that different doses of GCs induced autophagy and apoptosis of bone cells [15]. Prolonged autophagy activity precipitates cell apoptosis [16]. The relationship between GC and autophagy in the femoral head articular cartilage of broilers is unclear

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