Abstract
Mangiferin is a naturally occurring xanthone C-glycoside that is widely found in various plants. Previous studies have reported that mangiferin inhibits tumor cell proliferation and migration. Excessive proliferation and migration of vascular smooth muscle cells (SMCs) is associated with neointimal hyperplasia in coronary arteries. However, the role and mechanism of mangiferin action in neointimal hyperplasia is still unknown. In this study, a mouse carotid artery ligation model was established, and primary rat smooth muscle cells were isolated and used for mechanistic assays. We found that mangiferin alleviated neointimal hyperplasia, inhibited proliferation and migration of SMCs, and promoted platelets derive growth factors-BB- (PDGF-BB-) induced contractile phenotype in SMCs. Moreover, mangiferin attenuated neointimal formation by inhibiting mitochondrial fission through the AMPK/Drp1 signaling pathway. These findings suggest that mangiferin has the potential to maintain vascular homeostasis and inhibit neointimal hyperplasia.
Highlights
Coronary artery disease (CAD) is a growing health burden worldwide [1]
Mangiferin exerted this effect by decreasing the phosphorylation of Drp1 at Ser616 and promoting mitochondrial fusion through AMPK activation. In line with this finding, we found that the inhibition of AMPK by compound C (CC) reversed the mangiferin-induced inhibition of neointima hyperplasia
This was consistent with findings from our study which showed that mangiferin increased AMPK phosphorylation in RSMCs treated with PDGF-BB
Summary
Coronary artery disease (CAD) is a growing health burden worldwide [1]. Neointimal hyperplasia of the coronary arteries is the major pathophysiological change associated with CAD [2]. Mangiferin has previously been shown to have antioxidant, antiinflammatory, and antitumor activities [15–18] It has been associated with the progression of various diseases by modulating mitochondrial function [19–21]. We demonstrated that mangiferin protects the arteries against neointima hyperplasia Mangiferin exerted this effect by decreasing the phosphorylation of Drp at Ser616 and promoting mitochondrial fusion through AMPK activation. In line with this finding, we found that the inhibition of AMPK by compound C (CC) reversed the mangiferin-induced inhibition of neointima hyperplasia. The positive effect of mangiferin is AMPK/Drp dependent These findings indicate for the first time that mangiferin attenuates neointimal hyperplasia through the AMPK/Drp axis and that mangiferin is a potential natural compound for the treatment of restenosis artery disease
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