Mangiferin Inhibits PDGF-BB-Induced Proliferation and Migration of Rat Vascular Smooth Muscle Cells and Alleviates Neointimal Formation in Mice through the AMPK/Drp1 Axis

Figure 7

Diagram of mangiferin restraining neointimal hyperplasia. In the normal condition, VSMCs maintain contraction type, which are crucial for maintaining the physiology function of the coronary artery. PDGF-BB potent induces cell proliferation, migration, and phenotype change of VSMCs during neointimal hyperplasia. In this study, PDGF-BB inhibited AMPK phosphorylation activation at Thr 172, Drp1 was phosphorylation activated at Ser616, and then, Drp1 recruits to mitochondria accelerating mitochondrial fission, subsequently, VSMCs in coronary artery transform from contraction type to synthesis type, ultimately, contributing to the neointimal formation. However, we found that mangiferin effectively reversed the effect of PDGF-BB-induced neointimal formation.