Apigenin inhibits macrophage pyroptosis through regulation of oxidative stress and the NF‐κB pathway and ameliorates atherosclerosis

Author:

Weng Xiuzhu12,Luo Xing12,Dai Xinyu12,Lv Ying12,Zhang Shan12,Bai Xiaoxuan12,Bao Xiaoyi12,Wang Ying12,Zhao Chen12,Zeng Ming12,Hu Sining12,Li Ji12,Jia Haibo12ORCID,Yu Bo12

Affiliation:

1. Department of Cardiology The Second Affiliated Hospital of Harbin Medical University Harbin People's Republic of China

2. National Key Laboratory of Frigid Zone Cardiovascular Diseases Harbin People's Republic of China

Abstract

AbstractPyroptosis plays an important role in inflammatory diseases such as viral hepatitis and atherosclerosis. Apigenin exhibits various bioactivities, particularly anti‐inflammation, but its effect on pyroptosis remains unclear. The aim of this study is to investigate the effect of apigenin on pyroptosis and explore its potential against inflammatory diseases. THP‐1 macrophages treated by lipopolysaccharides/adenosine 5′‐triphosphate were used as the in vitro pyroptosis model. Western blot was used to detect the expression of NLRP3 inflammasome components and key regulators. Immunofluorescence was used to observe ROS production and intracellular location of p65. The potential of apigenin against inflammatory diseases was evaluated using atherosclerotic mice. Plaque progression was observed by pathological staining. Immunofluorescence was used to observe the expression of NLRP3 inflammasome components in plaques. The results showed that apigenin inhibited NLRP3 inflammasome activation. Apigenin reduced ROS overproduction and inhibited p65 nuclear translocation. Additionally, apigenin decreased the expression of NLRP3 inflammasome components in the plaque. Plaque progression was inhibited by apigenin. In conclusion, apigenin exhibited a preventive effect on macrophage pyroptosis by reducing oxidative stress and inhibiting the NF‐κB pathway. Apigenin may alleviate atherosclerosis at least partially by inhibiting macrophage pyroptosis. These findings suggest apigenin to be a promising therapeutic agent for inflammatory diseases.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Pharmacology

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