Baicalin Modulates CDH11/Wnt/α-catenin Pathway: A Novel Therapeutic Strategy Against Tibial Dyschondroplasia in Broiler Chickens.
Uloženo v:
| Název: | Baicalin Modulates CDH11/Wnt/α-catenin Pathway: A Novel Therapeutic Strategy Against Tibial Dyschondroplasia in Broiler Chickens. |
|---|---|
| Autoři: | Liu, Kai1,2, Mehmood, Khalid3 khalid.mehmood@iub.edu.pk, Li, Ying1, Sun, Yongxue1, Li, Aoyun4 aoyunli@henau.edu.cn, Zhang, Hui1,2 hz236@scau.edu.cn |
| Zdroj: | Pakistan Veterinary Journal. 2025, Vol. 45 Issue 3, p1146-1156. 11p. |
| Druh dokumentu: | Article |
| Témata: | Wnt signal transduction, Broiler chickens, Bone remodeling, Cartilage diseases, Metabolic bone disorders, Anti-inflammatory agents, Cadherins, Cartilage cells |
| Author-Supplied Keywords: | CDH11 Chondrocyte differentiation Tibial dyschondroplasia Wnt/α-catenin |
| Abstrakt: | Tibial dyschondroplasia (TD) is a metabolic cartilage disorder in fast-growing broilers, which severely impacts poultry welfare and productivity. Baicalin is a bioactive flavonoid with anti-inflammatory and antioxidant properties; its therapeutic potential has not been studied for TD. This study paves the way in elucidating baicalin's chondroprotective mechanism through CDH11/Wnt/β-catenin signaling and evaluating its therapeutic efficacy. Notably, baicalin significantly improved TD broilers' symptoms (e.g., slow weight-gain, reduced feed intake) and up-regulated tibia morphometrics. Special staining showed abnormal cartilage enlargement in TD and self-healing groups, while histomorphometry indicated restored tibial trabecular architecture in treated groups. Mechanistically, the cartilage development-related genes CDH11, RUNX2, and alkaline phosphatase (ALP) were significantly upregulated in the baicalin-treated group, and pivotal molecular factors in the Wnt/β-catenin-dependent signaling axis, which are involved in cartilage development, were up-regulated or down-regulated. These findings establish that baicalin mitigates TD pathogenesis through CDH11-dependent activation of canonical Wnt signaling, promoting chondrocyte maturation and skeletal remodeling, which will provide both mechanistic insights into avian skeletal metabolism and a clinically translatable strategy for metabolic bone diseases. [ABSTRACT FROM AUTHOR] |
| Copyright of Pakistan Veterinary Journal is the property of Pakistan Veterinary Journal, Faculty of Veterinary Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Author Affiliations: | 1College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China 2College of Animal Science, XiZang Agriculture and Animal Husbandry University, Linzhi 860000, China 3Faculty of Veterinary and Animal Sciences, Islamia University of Bahawalpur, Pakistan 4College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450002, China |
| ISSN: | 0253-8318 |
| DOI: | 10.29261/pakvetj/2025.224 |
| Přístupové číslo: | 188868428 |
| Databáze: | Veterinary Source |
| Abstrakt: | Tibial dyschondroplasia (TD) is a metabolic cartilage disorder in fast-growing broilers, which severely impacts poultry welfare and productivity. Baicalin is a bioactive flavonoid with anti-inflammatory and antioxidant properties; its therapeutic potential has not been studied for TD. This study paves the way in elucidating baicalin's chondroprotective mechanism through CDH11/Wnt/β-catenin signaling and evaluating its therapeutic efficacy. Notably, baicalin significantly improved TD broilers' symptoms (e.g., slow weight-gain, reduced feed intake) and up-regulated tibia morphometrics. Special staining showed abnormal cartilage enlargement in TD and self-healing groups, while histomorphometry indicated restored tibial trabecular architecture in treated groups. Mechanistically, the cartilage development-related genes CDH11, RUNX2, and alkaline phosphatase (ALP) were significantly upregulated in the baicalin-treated group, and pivotal molecular factors in the Wnt/β-catenin-dependent signaling axis, which are involved in cartilage development, were up-regulated or down-regulated. These findings establish that baicalin mitigates TD pathogenesis through CDH11-dependent activation of canonical Wnt signaling, promoting chondrocyte maturation and skeletal remodeling, which will provide both mechanistic insights into avian skeletal metabolism and a clinically translatable strategy for metabolic bone diseases. [ABSTRACT FROM AUTHOR] |
|---|---|
| ISSN: | 02538318 |
| DOI: | 10.29261/pakvetj/2025.224 |