Exploratory experiment designed to discover new patterns targeting Cx43 in H₂O₂-treated chondrocytes with Gap26 inhibitor. Primary outcome: Reduced hemichannel opening and suppressed Wnt signaling
A pharmacological intervention study using Gap26, a specific Connexin 43 inhibitor, to investigate the functional role of Cx43 in chondrocyte responses to oxidative stress. The study examined whether blocking Cx43 hemichannel function could prevent or reduce oxidative stress-induced degenerative changes, Wnt/β-catenin signaling activation, and extracellular matrix degradation in the cellular model of TMJOA.
Treatment of chondrocytes with Gap26 inhibitor followed by H₂O₂-induced oxidative stress, assessment of hemichannel function, Wnt/β-catenin signaling, and degenerative markers
Gap26 would reduce hemichannel opening, suppress Wnt signaling, and mitigate degenerative changes
Demonstration of reduced hemichannel activity, decreased Wnt/β-catenin signaling, and protection against degenerative changes
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