Baicalin Inhibits VSMC Phenotypic Transition and Ameliorates Atherosclerosis via GSK3β-TCF21 Signaling Pathway

Background Atherosclerosis (AS) is the pathological basis of acute myocardial infarction, acute stroke, and other acute critical illnesses. Vascular smooth muscle cell (VSMC) phenotypic transformation plays a remarkable role in the occurrence and development of AS. Previous studies have found that GSK3β-TCF21 is a key signaling pathway regulating VSMC phenotypic transformation. Baicalin is an important herbal monomer for cardiovascular protection, but whether it can regulate the GSK3β-TCF21 signaling pathway and VSMC phenotypic transformation remains unclear. Purpose The study aimed to explore the role of Baicalin in AS and VSMC phenotypic transformation and whether the GSK3β-TCF21 signaling pathway participates in this process. Materials and Methods In this study, through the AS mouse model and ox-LDL-induced VSMC phenotypic transformation model in vitro, the effect of Baicalin on the GSK3β-TCF21 signaling pathway and VSMC phenotypic transformation was investigated. Results Pathological staining showed that the AS plaque area of the Baicalin group decreased significantly ( p < 0.001). The expression of the marker gene (TAGLN, ACTA2, CNN1, and MYH11) of VSMC phenotypic transformation was significantly increased ( p < 0.001) after Baicalin treatment. Baicalin could activate GSK3β and increase the expression of TCF21 significantly ( p < 0.001) to inhibit VSMC phenotypic transition. Inhibiting the GSK3β-TCF21 signaling pathway was able to reduce the effects of Baicalin on reducing VSMC phenotypic transition and protecting AS. Conclusion Our study indicates that Baicalin is protective in inhibiting VSMC phenotypic transformation and ameliorating AS by regulating GSK3β-TCF21.