Abstract
ObjectiveOral submucous fibrosis (OSF) is a chronic, insidious, progressive mucosal disease that may be affected by mutations in the Wnt/β-catenin signaling pathway. Panax notoginseng saponins (PNS) is a powerful anti-fibrosis agent; however, its effect and mechanism in treating OSF remain unclear. This study investigated the effect and mechanism of PNS treatment for OSF. Study DesignArecoline was used to induce OSF models in vivo and in vitro, which were then treated with PNS. Hematoxylin-eosin (HE) and Masson trichrome staining were used to observe histopathology changes; E-cadherin and β-catenin were detected by Immunohistochemical assay, and type Ⅰ collagen (CollA1) and β-catenin were detected by immunofluorescent staining. The Wnt/β-catenin pathway and fibrosis signs were assessed using Western Blot and real-time quantitative polymerase chain reaction (RT-qPCR). ResultsThe expression of CollA1, Wnt1, and β-catenin were increased, and E-cadherin, GSK-3β, and β-catenin expression were decreased in OSF models. PNS and inhibitor intervention increased E-cadherin, Wnt1, and β-catenin, and decreased CollA1 and GSK-3β in a dose-dependent manner. ConclusionPNS can improve OSF by inhibiting the Wnt/β-catenin signal pathway and thus may be used as a potential medicine for the treatment of OSF.
Published Version
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