1Yunnan
Qujing Normal University, College of Biological and Food
Engineering, 655011 Yunnan, China;
2College
of Veterinary Medicine, Huazhong Agricultural
University, Wuhan, 430070, China; 3Department
of Biochemistry, College of Science, King Saud
University, PO Box 2455, Riyadh 11451, Saudi Arabia.
Tibial dyschondroplasia (TD) is a prevalent skeletal
disorder of rapidly growing broilers characterized by an
avascular, non-mineralized cartilage plug in the
proximal tibiotarsal growth plate and by failure of
endochondral ossification; its genome-wide molecular
signature and druggable nodes remain incompletely
defined. This study integrated histopathology,
micro-computed tomography, RNA sequencing and in-vivo
and in-vitro genetic approaches to characterize
the TD transcriptome and to determine whether baicalin,
a flavone glucuronide from Scutellaria baicalensis,
ameliorates TD through the cadherin-11 (CDH11)/Wnt/β-catenin
axis. One-day-old Arbor Acres broilers (n = 240) were
allocated to control (Con), TD, and baicalin (BA)
groups; TD and BA birds received 100mg/kg thiram from d
4 to 7 and BA birds received 200mg/kg baicalin from d 8
to 18. TD birds exhibited growth plate thickening, an
avascular cartilage plug, proteoglycan depletion,
lameness and reduced growth. Baicalin reduced the TD
incidence index by 58.4%, normalized growth plate
architecture and restored trabecular bone volume. RNA-seq
identified 2,847 differentially expressed genes (DEGs)
between TD and Con, with gene ontology, KEGG and gene
set enrichment analyses converging on suppression of Wnt/β-catenin
signaling, chondrocyte differentiation and matrix
organization; 66.4% of baicalin-responsive DEGs reverted
toward control levels. Quantitative PCR confirmed
coordinated suppression of CDH11, WNT3A and CTNNB1 with
induction of GSK3B, MMP13, ADAMTS5 and CASP9 in TD, all
reversed by baicalin. In primary chondrocytes, baicalin
(20μM) reversed thiram-induced loss of viability,
apoptosis and cell-cycle arrest; restored β-catenin
nuclear translocation and TOPFlash reporter activity;
and CDH11 knockdown abolished these effects. These
findings identify suppression of CDH11-dependent Wnt/β-catenin
signaling as a central molecular signature of TD and
demonstrate that baicalin is a therapeutically
effective, pathway-targeted intervention within the
18-day experimental period. However, long-term effects
on bone mechanical strength, persistence of recovery
after treatment withdrawal, and practical dietary safety
were not evaluated. Therefore, baicalin should be
considered a promising candidate requiring further
long-term validation before application in commercial
broiler production.
To Cite This Article:
Yuan H, Yang W, Lu K, Chen L, Xia S, Yang S, Sun Q,
Pan L, Ataya FS and
Li Z, 2026. Pathological and transcriptomic signatures
of tibial dyschondroplasia and the therapeutic potential
of baicalin via the CDH11/Wnt/β-catenin axis. Pak Vet J,
2026, 46(10): 2443-2455.
http://dx.doi.org/10.29261/pakvetj/2026.251