Abstract

Background: Aortic dissection (AD) is a lethal vascular disease caused by the formation of hematoma in the middle layer of the aortic wall. Inflammation and oxidative stress play important roles in the development of AD. Galectin-3 (Gal-3) is a 26-kDa lectin recognized to regulate many aspects of inflammatory cell behavior. Modified citrus pectin (MCP) is a pH-modified form of the dietary soluble citrus peel fiber known as pectin. It is abundant in β-galactose, which allows it to bind to Gal-3, and is recommended as a therapeutic agent for immune support, cancer, toxicity, and fibrotic diseases. The aim of this study was to explore the effect of MCP on AD and its potential mechanism involved. Methods and Results: MCP (100mg/kg) was orally administrated once every two days to retard the development of 3-aminopropionitrile fumarate/angiotensin II-induced AD animal models. In vivo, AD aorta presented an increase in Gal-3 levels that were accompanied by an increase in macrophage. Treatment with MCP decreased the incidence and mortality of AD by reducing inflammatory cell infiltration to the aorta; it downregulated the gene expression of inflammation and pyroptosis, such as IL-6, TNF-α, NLRP3, caspase-1, and IL-1β. In vitro, MCP could inhibit macrophage pyroptosis in H 2 O 2 -stimulated Raw264.7 cells. Additionally, Gal-3 is directly bound to TLR4 in H 2 O 2 -induced macrophages but MCP almost completely disrupted their interaction and suppressed activation of NF-KB by co-immunoprecipitation assays. Conclusions: Gal-3 could be a new molecular mechanism associated with AD disease, implying the use of MCP as a promising therapeutic strategy to prevent AD development.

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