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ORIGINAL PAPER
Dietary catalpol reduces T-2 toxin-induced cartilage damage
via p38MAPK/NF-κB/IAPs pathway inhibition in Wistar rats
1
Harbin Medical University, Chinese Center for Disease Control and Prevention, Center for Endemic Disease Control,
Harbin city, Heilongjiang Province, 150081, PR China
Publication date: 2026-06-15
Corresponding author
K. Wang
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, PR China
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, PR China
KEYWORDS
TOPICS
ABSTRACT
This study aimed to evaluate therapeutic effects, including
bactericidal and anti-inflammatory activity, inhibition of oxidative damage,
neuroprotection, hepatoprotection, and suppression of hyperglycaemia.
However, the protective effect of catalpol on T-2 toxin-induced cartilage damage
remains unclear. The present results demonstrate that T-2 toxin causes
increased chondrocyte apoptosis, leading to reduced survival of these cells. It
also contributes to extracellular matrix degradation by decreasing collagen II
expression and elevating matrix metalloproteinase 13 expression. Furthermore,
T-2 toxin activates the p38MAPK/NF-κB/IAPs signalling pathway and induces a
dose-dependent inflammatory response in chondrocytes, reflected by elevated
levels of inflammation-related mediators. Additionally, catalpol reduces T-2
toxin-induced chondrocyte apoptosis and inflammatory response by regulating
the p38MAPK/NF-κB/IAPs signalling pathway. These findings elucidate the
molecular mechanism underlying chondrocyte damage caused by T-2 toxin
exposure and identify potential therapeutic targets, providing a theoretical basis
for the use of catalpol in the treatment of T-2 toxin-induced cartilage damage.
FUNDING
This study was supported by the State Administration of Foreign Experts Affairs (20172300014).
CONFLICT OF INTEREST
The Authors declare that there is no conflict of interest.
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