ArticleCytotechnology2026
Angelica sinensis polysaccharide reduces macrophage FPR2 to regulate the hepatic inflammatory microenvironment and activate the PI3K/AKT signaling pathway to improve insulin resistance.
Article in Cytotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Angelica sinensis polysaccharide (ASP) is one of the main active components of Angelica sinensis and has a significant ameliorative effect on high-fat diet (HFD)-induced insulin resistance (IR). This study aims to investigate the effect of ASP on IR and its mechanism. The in vivo IR model was established by HFD feeding in SD rats, and the in vitro IR model was constructed by insulin treatment in HepG2 cells. Fasting insulin levels were detected using assay kits; intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test (IPITT) were used to evaluate the metabolic responses to glucose and insulin loads, respectively. HE staining was performed to observe pathological changes in liver tissues. RT-qPCR, Western blot, immunofluorescence, immunohistochemistry, and ELISA were employed to detect key genes and proteins expression. HFD rats showed significantly increased body weight, fasting blood glucose, insulin levels, and FPR2 expression. FPR2 knockdown alleviated pathological damage in liver tissues, reduced the expression of glucose metabolism-related genes G6pase, PEPCK, and GSK3β, and mitigated IR in HFD rats, and inhibited LPS-induced M1 polarization of macrophages, promoted M2 polarization. Mechanistically, treatment with LPS-induced macrophage culture medium reduced glucose uptake capacity and PI3K/AKT pathway activity in HepG2-IR cells, increased extracellular glucose content, and upregulated glucose metabolism-related gene expression. However, treatment with culture medium from FPR2-knockdown and LPS-induced macrophages reversed these abnormalities. Further treatment with the PI3K inhibitor LY294002 blocked this protective effect. Additionally, ASP treatment reduces HFD-induced FPR2 expression, restored PI3K/AKT pathway activity, alleviated IR in HFD rats, and FPR2 overexpression weakened the protective effects of ASP. ASP improves IR in rats by downregulating FPR2 expression, inhibiting M1 macrophage-mediated hepatocyte inflammatory responses, and activating the PI3K/AKT signaling pathway. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01071-y.
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