## 1 Introduction  
Chronic inflammation of the arterial wall contributes critically to the formation of atherosclerosis [1]. Atherosclerosis features gradual lipids and accumulation of immune cells in the arterial intima, which can lead to acute clinical outcomes including myocardial infarction and ischemic stroke [2]. Lipid deposition at specific arterial wall sites initiates atheroma pathogenesis. As the disease progresses, the intimal layer undergoes multiple stages of inflammation, necrosis, fibrosis, and calcification and results in plaque formation [3]. The formation of cholesterol-laden macrophage-derived foam cells is critical in these stages [4]. Foam cells have lower mobility and produce proinflammatory cytokines and chemokines to recruit additional monocytes, T cells, and neutrophils, thus amplifyingthe inflammatory cascade [5]. In addition to immune cells, vascular smooth muscle cells (VSMCs) are pivotal in this vascular inflammatory disease.  
VSMCs are usually quiescent and differentiated in the \"contractile\" phenotype, where they maintain hemodynamics and vascular wall structure [6]. However, VSMCs also exhibit high dedifferentiation in response to stimulators such as inflammatory mediators, growth factors, extracellular matrix, and lipoproteins [7]. Dedifferentiated VSMCs, referred to as the \"synthetic\" phenotype, can proliferate, migrate, and express macrophage markers and thus demonstrate inflammatory properties, such as cytokine or chemoattractant production [8]. Lipid accumulation may be critical in the switch of VSMCs into macrophage-like cells. Cholesterol loading to VSMCs was observed to stimulate many proinflammatory genes and reduce the expression of VSMC marker genes [9]. These VSMC-derived macrophage-like cells are unlike typical immune cells: They have low phagocytic capacity but promote atherosclerosis pathogenesis by exacerbating vascular inflammation [10].  
Oxidized low-density lipoprotein (ox-LDL), considered as a main cause of atherosclerosis [11; 12], contributes to lipid accumulation in the intimal layer, which leads to the subsequent atherosclerosis event [13]. Lectin-like ox-LDL receptor \(1\) (LOX-1) is the major scavenger receptor of ox-LDL in endothelial cells [13]. However, it is not identified only in endothelial cells but also in macrophages and VSMCs [13]. Furthermore, the binding of ox-LDL to LOX-1 enhances the expression of monocyte chemoattractant protein-1 (MCP-1) [14], which is critical in the pathogenesis of inflammatory diseases, including cancer and atherosclerosis [15]. Together with proinflammatory cytokines, ox-LDL thus contributes to atherosclerosis pathogenesis. Therefore, the inhibition of proinflammatory factors (and the subsequent inflammatory cascade) may be effective in atherosclerosis therapy.  
Platonin (Figure 1A), a cyanine photosensitizing dye with immunomodulating activity, is currently used in clinics to treat immune diseases such as rheumatoid arthritis [16]. Platonin exhibits free radical scavenging activity and can inhibit the production of inflammatory mediators including interleukin (IL)-6, IL-18, and tumor necrosis factor \(\alpha\), and the expression of inducible nitric oxide synthase (iNOS) in lipopolysaccharideacharide (LPS)-activated macrophages [17; 18]. Platonin can also diminish circulatory failure and increase the survival rate of septic rats [19]. A recent study reported that platonin can prevent injury due to macrophage-mediated inflammatory responses in the brain [20]. Considering the critical role of inflammatory VSMCs in atherosclerosis pathogenesis, the anti-inflammatory effects and possible underlying mechanisms of platonin in VSMCs treated with different stimulators were determined in the present study. The treatment of platonin may be a potential for treating vascular diseases in clinical application due to its possible anti-inflammatory capacity in VSMCs.