Protective mechanism of tetramethylpyrazine on cardiovascular system.
10.19540/j.cnki.cjcmm.20221012.402
- Author:
Chun-Kun YANG
1
;
Qing-Quan PAN
2
;
Kui JI
2
;
Chuan-Chao LUO
2
;
Zhuang TIAN
2
;
Hong-Yuan ZHOU
2
;
Jun LI
1
Author Information
1. Guang'anmen Hospital, China Academy of Chinese Medical Sciences Beijing 100053, China.
2. Department of Emergency, Weifang Hospital of Traditional Chinese Medicine Weifang 261041, China.
- Publication Type:Journal Article
- Keywords:
inflammation;
ischemia/reperfusion;
lipid;
tetramethylpyrazine;
thrombus;
vascular endothelial cells;
vascular smooth muscle cells
- MeSH:
Mice;
Animals;
Endothelial Cells/metabolism*;
Phosphatidylinositol 3-Kinases/metabolism*;
Myocardial Infarction;
Myocardium/metabolism*;
Myocytes, Cardiac;
Thrombosis;
Inflammation;
Apoptosis
- From:
China Journal of Chinese Materia Medica
2023;48(6):1446-1454
- CountryChina
- Language:Chinese
-
Abstract:
Tetramethylpyrazine is the main component of Ligusticum chuanxiong. Studies have found that tetramethylpyrazine has a good protective effect against cardiovascular diseases. In the heart, tetramethylpyrazine can reduce myocardial ischemia/reperfusion injury by inhibiting oxidative stress, regulating autophagy, and inhibiting cardiomyocyte apoptosis. Tetramethylpyrazine can also reduce the damage of cardiomyocytes caused by inflammation, relieve the fibrosis and hypertrophy of cardiomyocytes in infarcted myocardium, and inhibit the expansion of the cardiac cavity after myocardial infarction. In addition, tetramethylpyrazine also has a protective effect on the improvement of familial dilated cardiomyopathy. Besides, the mechanisms of tetramethylpyrazine on blood vessels are more abundant. It can inhibit endothelial cell apoptosis by reducing oxidative stress, maintain vascular endothelial function and homeostasis by inhibiting inflammation and glycocalyx degradation, and protect vascular endothelial cells by reducing iron overload. Tetramethylpyrazine also has a certain inhibitory effect on thrombosis. It can play an anti-thrombotic effect by reducing inflammatory factors and adhesion molecules, inhibiting platelet aggregation, and suppressing the expression of fibrinogen and von Willebrand factor. In addition, tetramethylpyrazine can also reduce the level of blood lipid in apolipoprotein E-deficient mice, inhibit the subcutaneous deposition of lipids, inhibit the transformation of macrophages into foam cells, and inhibit the proliferation and migration of vascular smooth muscle cells, thereby reducing the formation of atherosclerotic plaque. In combination with network pharmacology, the protective mechanism of tetramethylpyrazine on the cardiovascular system may be mainly achieved through the regulation of phosphatidylinositol 3 kinase/protein kinase B(PI3K/Akt), hypoxia-inducible factor 1(HIF-1), and mitogen-activated protein kinase(MAPK) pathways. Tetramethylpyrazine hydrochloride and sodium chloride injection has been approved for clinical application, but some adverse reactions have been found in clinical application, which need to be paid attention to.
