Abstract
Astragaloside IV (AS-IV) is the main active compound of Astragalus membranaceus. In this study, we investigated whether AS-IV could attenuate atherosclerosis and hepatic steatosis in LDLR−/−mice and its potential mechanisms. After 12 weeks of high fat diet, the LDLR−/−mice were randomly divided into four groups. Then, the mice were administrated with 0.9% saline or AS-IV (10 mg/kg) or atorvastatin (1.3 mg/kg) for 12 weeks. Serum lipid profiles and inflammatory cytokines were detected by ELISA, hepatic TC and TG by colorimetric enzymatic kits, gene expression by RT-qPCR, plaque sizes by H&E staining, Oil Red O, liver pathology by H&E staining, collagen content by Masson, α-SMA, caspase-3 and NF-κB p65 production by immunofluorescence staining. MAPK/NF-κB pathway and inflammation related proteins were detected by Western Blot. The results showed that AS-IV decreased the levels of serum lipids, reduced plaque area and increased plaque stability in HFD-induced LDLR−/− mice. AS-IV also decreased the levels of inflammatory cytokines in the serum, aortas and liver tissue, and NF-κB p65 in aortic roots. The phosphorylation of JNK, ERK1/2, p38 and NF-κB, and inflammatory proteins (iNOS, VCAM-1and IL-6) was inhibited in AS-IV-treated group. In summary, AS-IV inhibited inflammation to attenuate atherosclerosis and hepatic steatosis via MAPK/NF-κB signaling pathway in LDLR−/− mice.
Highlights
Atherosclerosis (AS) is the pathological basis of a variety of cardiovascular diseases (CVDs) (Roth et al, 2017)
Astragaloside IV (AS-IV) is a type of polysaccharide extracted from Astragalus membranaceus, which is a traditional Chinese herbal medicine for CVD (Zhang et al, 2011; Ma et al, 2013)
We investigated whether ASIV could alleviate AS and hepatic steatosis, and uncovered the underlying mechanism
Summary
Atherosclerosis (AS) is the pathological basis of a variety of cardiovascular diseases (CVDs) (Roth et al, 2017). As a lipid-driven inflammatory disease within the arterial wall, AS is always treated with lipidlowering and anti-inflammatory therapies (Taleb, 2016). It is necessary to find more effective methods to prevent and treat AS. Dyslipidemia, inflammation, and oxidative stress closely link AS with nonalcoholic fatty liver disease (NAFLD). The prevalence of NAFLD has been estimated to be 20–30% in the general population, and associated with several cardiovascular risk factors (Targher et al, 2008). A study has found that the prevalence of CVD is higher in patients with NAFLD (Targher et al, 2010a). NAFLD patients were found to have higher levels of subclinical
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