Mechanism of Buyang Huanwu Decoction glycosides against atherosclerotic inflammation through NF-κB signaling pathway.
10.19540/j.cnki.cjcmm.20220905.703
- Author:
Xin-Ying FU
1
;
Zheng-Ji SUN
2
;
Qing-Yin LONG
1
;
Wei TAN
1
;
Yan-Jun LI
1
;
Lu WU
3
;
Qing-Hu HE
4
;
Wei ZHANG
1
Author Information
1. Hunan Provincial Key Laboratory of Cardiovascular and Cerebrovascular Prevention and Treatment of Integrated Traditional Chinese and Western Medicine,Hunan University of Chinese Medicine Changsha 410208,China.
2. Yueyang Hospital of Traditional Chinese Medicine Yueyang 414021,China.
3. Liuyang Hospital of Traditional Chinese Medicine Liuyang 410399,China.
4. Hunan University of Medicine Huaihua 418000,China.
- Publication Type:Journal Article
- Keywords:
Buyang Huanwu Decoction;
NF-κB signaling pathway;
atherosclerosis;
glycosides;
inflammatory response
- MeSH:
Mice;
Animals;
NF-kappa B/metabolism*;
NF-KappaB Inhibitor alpha/metabolism*;
Tumor Necrosis Factor-alpha/metabolism*;
Glycosides/pharmacology*;
Cholesterol, LDL;
Atherosclerosis/genetics*;
Signal Transduction;
Inflammation/drug therapy*;
Interleukin-6;
Apolipoproteins E/pharmacology*;
RNA, Messenger/metabolism*
- From:
China Journal of Chinese Materia Medica
2023;48(1):202-210
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to explore the effect of Buyang Huanwu Decoction glycosides on the inflammatory response of apolipoprotein E~(-/-)(ApoE~(-/-)) mice and RAW264.7 cells through nuclear factor kappa-B(NF-κB) signaling pathway. In the in vivo experiment, ApoE~(-/-) mice were fed with high-fat diets for 12 weeks to induce the animal model of atherosclerosis, and 75 μg·mL~(-1) oxidized low-density lipoprotein(Ox-LDL) incubated RAW264.7 cells for 24 h to establish the atherosclerosis cell model. Automatic biochemical analyzer, hematoxylin-eosin(HE) staining, enzyme-linked immunosorbent assay(ELISA), Western blot, and droplet digital polymerase chain reaction(PCR) were used to determine the blood lipid levels, aortic intimal thickness, inflammatory factor content, NF-κB pathway-related proteins, and mRNA expression levels, and evaluate arterial atherosclerotic lesions and anti-atherosclerotic mechanisms of the drug. The model of atherosclerosis was successfully established in ApoE~(-/-) mice after 12 weeks of feeding with high-fat diets. In the model group, the plasma levels of total cholesterol(TC), triglyceride(TG), and low-density lipoprotein cholesterol(LDL-C) were increased(P<0.01), the intima of the blood vessels was thickened, the levels of inflammatory factors tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) were increased, and the protein and mRNA expressions of NF-κB and inhibitor of NF-κB(IκBα) were significantly increased as compared with the control group. Compared with the model group, the high-dose Buyang Huanwu Decoction glycoside group decreased the plasma levels of TC, TG, and LDL-C, reduced the plaque area and thickness and the content of inflammatory factor TNF-α, and inhibited the protein and mRNA expressions of NF-κB and IκBα, with the effect same as Buyang Huanwu Decoction. In the in vivo experiment, 75 μg·mL~(-1) Ox-LDL stimulated RAW264.7 cells for 24 h to successfully establish a foam cell model. As compared with the control group, the nuclear amount of NF-κB and the protein and mRNA expressions of IκBα in the model group increased. Compared with the model group, the middle-dose and high-dose Buyang Huanwu Decoction glycoside groups decreased the nuclear amount of NF-κB and the protein and mRNA expressions of IκBα. The above results show that the glycosides are the main effective substances of Buyang Huanwu Decoction against atherosclerosis, which inhibit the NF-κB pathway and reduce the inflammatory response, thus playing the role against atherosclerotic inflammation same as Buyang Huanwu Decoction.