The Role and Molecular Mechanism of Ginsenoside Rb1 in the Attenuation of Atherosclerosis through Suppression of Neutrophil Extracellular Trap Formation
- VernacularTitle:人参皂苷Rb1抑制NETs形成防治动脉粥样硬化的作用及分子机制
- Author:
Zhenni YANG
1
;
Zilong ZHANG
;
Jingang CUI
;
Xiaoye DU
;
Jing XU
;
Minqi XIONG
;
Yu CHEN
;
Teng ZHANG
Author Information
- Publication Type:Journal Article
- Keywords: Ginsenoside Rb1; Neutrophil extracellular trap network; Atherosclerosis; Cholesterol crystal; Oxidative stress; Histone citrullination
- From: World Science and Technology-Modernization of Traditional Chinese Medicine 2025;27(10):2889-2898
- CountryChina
- Language:Chinese
- Abstract: Objective To investigate the role and molecular mechanism of ginsenoside Rb1(Rb1)in regulating neutrophil extracellular trapping networks(NETs)to intervene in atherosclerosis(AS).Methods In vivo:an AS model was constructed with ApoE knockout mice superimposed on a high-fat diet.The pathological and morphological changes of aortic root plaques were observed by HE staining and oil red O staining;Immunofluorescence labelling of neutrophils citrullinated histones(Cit-H3)and macrophages as well as IL-1β at the aortic root plaque site were used to assess the inflammatory infiltration.In vitro:NETs induced by PMA and cholesterol crystals were taken as models respectively.Direct effect of Rb1 against NETs formation assessed by Sytox staining and immunofluorescence staining with Cit-H3 and myeloperoxidase.Rb1 on ROS levels was assessed by DCFH-DA.Rb1 on histone H3 citrulline modification was assessed by Western blotting.Results In vivo:Rb1 significantly inhibited plaque formation,lipid deposition(P<0.05)and intra-plaque inflammatory infiltration(P<0.05).In vitro:Rb1 significantly inhibited NETs formation(P<0.05),neutrophil ROS levels(P<0.05),and Cit-H3 levels(P<0.05).Conclusions Rb1 significantly inhibited AS progression by inhibiting plaque NETs formation,which may be partly through the inhibition of histone H3 citrullination resulting from activation of the neutrophil oxidative stress pathway.
