College of Animal Science and Veterinary Medicine, Shandong Agricultural University, 61 Daizong Street, Tai'an City, 271018, Shandong Province, China.
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, 271018, Shandong Province, China.
Biol Trace Elem Res. 2022 Jul;200(7):3326-3335. doi: 10.1007/s12011-021-02921-w. Epub 2021 Sep 21.
Manganese (Mn) is a crucial trace element for poultry nutrition, and its deficiency compromises tibial cartilage development, leading to perosis and a higher incidence of slipped tendon. Tibial dyschondroplasia (TD) is a metabolic cartilage disease characterized by disruption of endochondral bone formation, which is closely related to extracellular matrix (ECM) degradation, in which Mn deficiency plays an important role. Previous studies have confirmed the role of matrix metalloproteinases (MMPs) in the pathogenesis of TD, but whether dysregulated ECM degradation and MMP expression profiles in growth plate are involved in Mn deficiency-induced avian TD has not been fully elucidated yet. Thus, this study was conducted to clarify these issues. Firstly, we successfully established TD model induced by Mn deficiency in broiler chicks. Mn deficiency decreased the number of chondrocytes, contents of proteoglycan, and type II collagen in tibial growth plate, demonstrating the tibial growth plate damage with enhanced ECM degradation. Also, Mn deficiency inhibited the Nrf2 signaling pathway and enhanced the protein levels of NLRP3, active caspase-1, and active IL-1β in tibial growth plate, indicating the oxidative stress and inflammatory response in Mn deficiency-induced TD. Additionally, upregulated expression levels of MMPs (MMP1, 9, and 13) were observed in tibial growth plate of Mn deficiency group. In summary, these findings suggest that Mn deficiency-enhanced ECM degradation is involved in avian TD, which may be correlated with oxidative stress, inflammatory response, and upregulation of MMPs.
锰（Mn）是家禽营养的重要微量元素，其缺乏会损害胫骨软骨的发育，导致骨软骨发育不良和腱滑脱的发病率增加。胫骨软骨发育不良（TD）是一种代谢性软骨疾病，其特征是破坏软骨内成骨，这与细胞外基质（ECM）降解密切相关，其中锰缺乏起着重要作用。先前的研究已经证实了基质金属蛋白酶（MMPs）在 TD 发病机制中的作用，但 ECM 降解和 MMP 表达谱的失调是否参与了锰缺乏诱导的禽类 TD 尚未完全阐明。因此，本研究旨在阐明这些问题。首先，我们成功建立了由锰缺乏引起的肉鸡 TD 模型。锰缺乏减少了胫骨生长板中的软骨细胞数量、蛋白聚糖含量和 II 型胶原含量，表明胫骨生长板损伤伴有增强的 ECM 降解。此外，锰缺乏抑制了 Nrf2 信号通路，并增加了胫骨生长板中 NLRP3、活性 caspase-1 和活性 IL-1β的蛋白水平，表明锰缺乏诱导的 TD 存在氧化应激和炎症反应。此外，在锰缺乏组的胫骨生长板中观察到 MMPs（MMP1、9 和 13）的表达水平上调。综上所述，这些发现表明，锰缺乏增强的 ECM 降解参与了禽类 TD，这可能与氧化应激、炎症反应和 MMPs 的上调有关。
