RETRACTED: Experimental study on the regulation of M1/M2 macrophage polarisation to improve atherosclerosis by Strengthening the Jian-Pi-Qu-Tan Formula

Abstract

Objective:To investigate the mechanism of action of Jian-Pi-Qu-Tan Formula in regulating the polarisation balance of M1/M2 type macrophages and attenuating atherosclerosis in ApoE-/-mice. Methods:Ten male SPF-grade C57BL/6J mice were used as the control group (Con group); male SPF-grade ApoE-/- mice, 30 mice, were randomly divided into the AS model group (Mod group), the Jian-Pi-Qu-Tan Formula group (JPQT group), and the atorvastatin calcium tablets group (ATO group) according to the random-number-table method, with 10 mice in each group. Among them, the CON group was given normal feed and the remaining group was given atherosclerotic feed. Gastric administration of drugs was started 8 weeks after modelling, and the corresponding drugs were given by gavage in the JPQT and ATO groups, and an equal amount of saline was given by gavage in the Con and Mod groups for 8 weeks. Body weight was continuously monitored, and after blood collection from the abdominal aorta, the serum TC and TG levels of mice in each group were compared; plaque formation in aortic tissues was observed by HE staining, oil red O staining and Masson staining; the expression levels of pro-inflammatory factors IL-6, IL-12 and anti-inflammatory factor IL-10 were detected by ELISA; and the positive expression of aortic CD86 and CD206 was detected by immunofluorescence; Western blot detected the protein expression levels of aortic iNOS, Arg-1, STAT6 and p-STAT6. Results:Jian-Pi-Qu-Tan Formula significantly improved lipid levels and inflammatory factor levels, attenuated atherosclerotic plaque formation, decreased iNOS protein levels, and increased Arg-1 and p-STAT6 protein levels, and regulated M1/M2 macrophage polarisation in ApoE-/-AS mice. Conclusion:Jian-Pi-Qu-Tan Formula regulates lipid metabolism, reduces inflammation and ameliorates atherosclerosis by activating STAT6 phosphorylation and regulating M1/M2 polarisation balance.