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Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway

Authors :
Li-Hua Wang
Zheng-Wei Gu
Jie Li
Wen-Qing Yang
Yun-Lun Li
Dong-Mei Qi
Dan-Yang Wang
Hai-Qiang Jiang
Source :
BMC Complementary Medicine and Therapies, Vol 23, Iss 1, Pp 1-11 (2023)
Publication Year :
2023
Publisher :
BMC, 2023.

Abstract

Abstract Background Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway. Methods (1) ApoE−/− mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test. Results (1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability. Conclusion Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration.

Details

Language :
English
ISSN :
26627671
Volume :
23
Issue :
1
Database :
Directory of Open Access Journals
Journal :
BMC Complementary Medicine and Therapies
Publication Type :
Academic Journal
Accession number :
edsdoj.392539a914ff490383dc1dc9e325e70f
Document Type :
article
Full Text :
https://doi.org/10.1186/s12906-023-03902-3