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Article Publish Status: FREE
Abstract Title:

Astragaloside IV Relieves Atherosclerosis and Hepatic SteatosisMAPK/NF-κB Signaling Pathway in LDLRMice.

Abstract Source:

Front Pharmacol. 2022 ;13:828161. Epub 2022 Feb 21. PMID: 35264962

Abstract Author(s):

Yifan Zhang, Min Du, Jiarou Wang, Ping Liu

Article Affiliation:

Yifan Zhang

Abstract:

Astragaloside IV (AS-IV) is the main active compound ofmembranaceus. 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 LDLRmice. 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 steatosisMAPK/NF-κB signaling pathway in LDLRmice.

Study Type : Animal Study

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