Lu Lu, Jin Cong, Dong Peng-Fei, Wang Zhen-Yong
College of Animal Science and Veterinary Medicine, Shandong Agricultural University, 61 Daizong Street, 271018, Tai'an City, Shandong Province, China.
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, 271018, Tai'an City, Shandong Province, China.
Vet Res Commun. 2022 Dec;46(4):1023-1032. doi: 10.1007/s11259-022-09950-3. Epub 2022 Jul 15.
Manganese (Mn) is an essential microelement for broiler breeding and its deficiency causes tibial dyschondroplasia (TD). Tibial growth plate (TGP) development and metaphyseal vascularization are crucial for tibia growth in fast-growing broiler chickens, but their roles in Mn deficiency-induced TD in chicks remain unclear. This study was designed to clarify this issue. A total of 36 one-day-old broilers were divided into the control group and Mn-deficiency (Mn-D) group, which were fed with a standard diet (60 mg Mn/kg) and Mn deficiency diet (22 mg Mn/kg) for 42 days, respectively. TGP and proximal tibial metaphysis were collected to perform the related assays. This study found that Mn deficiency decreased the tibia length and TGP thickness in the TD model. Also, Mn deficiency increased the irregular and white tibial dyschondroplasia lesions (TDL) region under the TGP, and reduced the expression levels of vascular endothelial growth factor (VEGF) and macrophage migration inhibitory factor (MIF). Combined with histological assessment, it was suggested that Manganese deficiency inhibited angiogenesis in the proximal tibial metaphysis. Meanwhile, Mn deficiency enhanced the expression levels of hypoxia-inducible factor-1 α (HIF-1α), autophagy-related protein 5 (ATG5), and microtubule-associated protein 1 light chain 3 β (LC3-II) in TGP, but decreased the expression level of SQSTM1 (P62), which suggested that autophagy was activated during this process. Collectively, these data indicate that HIF-1α up-regulation and concurrent autophagy activation exert a protective effect against Mn deficiency-induced angiogenesis inhibition, which may provide useful guidance to prevent TD in broilers.
锰（Mn）是肉鸡养殖所必需的微量元素，其缺乏会导致胫骨软骨发育不良（TD）。胫骨生长板（TGP）发育和干骺端血管生成对于快速生长的肉鸡胫骨生长至关重要，但其在雏鸡锰缺乏诱导的TD中的作用仍不清楚。本研究旨在阐明这一问题。总共36只1日龄肉鸡被分为对照组和锰缺乏（Mn-D）组，分别用标准日粮（60毫克锰/千克）和锰缺乏日粮（22毫克锰/千克）喂养42天。收集TGP和胫骨近端干骺端进行相关检测。本研究发现，在TD模型中，锰缺乏会降低胫骨长度和TGP厚度。此外，锰缺乏会增加TGP下方不规则的白色胫骨软骨发育不良病变（TDL）区域，并降低血管内皮生长因子（VEGF）和巨噬细胞迁移抑制因子（MIF）的表达水平。结合组织学评估，提示锰缺乏抑制了胫骨近端干骺端的血管生成。同时，锰缺乏增强了TGP中缺氧诱导因子-1α（HIF-1α）、自噬相关蛋白5（ATG5）和微管相关蛋白1轻链3β（LC3-II）的表达水平，但降低了SQSTM1（P62）的表达水平，这表明在此过程中自噬被激活。总体而言，这些数据表明HIF-1α上调和同时发生的自噬激活对锰缺乏诱导的血管生成抑制发挥了保护作用，这可能为预防肉鸡TD提供有用的指导。
