Gegen Qinliantang Regulates Polarization Tendency of Macrophages to Intervene in Vulnerable Plaque in AS of ApoE-/- Mice
10.13422/j.cnki.syfjx.20220418
- VernacularTitle:葛根芩连汤调控巨噬细胞极化趋势干预ApoE-/-小鼠动脉粥样硬化易损斑块机制
- Author:
Yi ZHENG
1
;
He GUO
1
;
Xi LUO
1
;
Yan-jie WANG
1
;
Dan-yu ZHAO
1
;
Lin ZHANG
1
;
Jing-yu WANG
1
;
Yu-xi LIU
1
;
Yong-rui BAO
1
;
Shuai WANG
1
;
Tian-jiao LI
1
;
Rui YU
1
;
Xian-sheng MENG
1
Author Information
1. Liaoning University of Traditional Chinese Medicine，Shenyang 110847，China
- Publication Type:Journal Article
- Keywords:
Gegen Qinliantang;
atherosclerosis;
macrophages;
polarization;
mechanism
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(11):60-69
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the mechanism underlying the intervention of Gegen Qinliantang （GQL） in vulnerable plaques in atherosclerosis （AS） of ApoE-/- mice by regulating the polarization of macrophages. MethodTwelve normal C57BL/6CNC mice were used as the control group， and 60 ApoE-/- mice of the same line were randomized into 5 groups： model group， low-dose， middle-dose， and high-dose GQL groups （GQL-D， GQL-Z， and GQL-G groups， respectively）， and atorvastatin group （western medicine group）. High-fat diet was used for modeling. The control group and the model group were given （ig） equal volume of sterile distilled water， and GQL-D， GQL-Z， GQL-G， and western medicine groups received （ig） corresponding concentration of drugs for 8 weeks. The levels of total cholesterol （TC）， triglyceride （TG）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） were detected with biochemical methods. The distribution of plaques in the aortic region was observed based on oil red O staining and hematoxylin-eosin （HE） staining. Serum levels of M1 pro-inflammatory factors tumor necrosis factor （TNF）-α and interleukin （IL）-6 and M2 anti-inflammatory factors IL-13 and transforming growth factor （TGF）-β were detected by enzyme-linked immunosorbent assay （ELISA）. Protein expression of macrophage mannose receptor CD206/arginase-1 （Arg-1） and CD206/inducible nitric oxide synthase （iNOS） was determined by double-labeling immunofluorescence， and mRNA expression of aortic Arg-1 and iNOS by real-time polymerase chain reaction （PCR）. ResultLevels of TG， TC， and LDL-C were significantly lower and HDL-C level was significantly higher in the GQL-Z， GQL-G， and western medicine groups than in the model group. As the concentration of GQL rose， the area with plaques gradually shrunk and the color became lighter. The staining areas of the GQL-G group and the western medicine group were the most scattered. The administration groups showed significant increase in the protein levels of Arg-1 and CD206， significant decrease in the protein level of iNOS， significant rise of Arg-1 mRNA level， and significant drop of iNOS mRNA level （P<0.05）. ConclusionGQL intervenes in the vulnerable plaques in AS by improving lipid metabolism， inhibiting macrophage M1 polarization， promoting macrophage M2 polarization， and further improving the inflammatory microenvironment.
