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Review
. 2021 May 13:12:675999.
doi: 10.3389/fphar.2021.675999. eCollection 2021.

Chinese Herbal Medicines and Active Metabolites: Potential Antioxidant Treatments for Atherosclerosis

Luxia Song  1   2 , Jie Zhang  1   2 , Runmin Lai  1   2 , Qiuyi Li  1   2 , Jianqing Ju  2 , Hao Xu  2
Affiliations
Review

Chinese Herbal Medicines and Active Metabolites: Potential Antioxidant Treatments for Atherosclerosis

Luxia Song et al. Front Pharmacol. .

Abstract

Atherosclerosis is a complex chronic disease that occurs in the arterial wall. Oxidative stress plays a crucial role in the occurrence and progression of atherosclerotic plaques. The dominance of oxidative stress over antioxidative capacity generates excess reactive oxygen species, leading to dysfunctions of the endothelium and accelerating atherosclerotic plaque progression. Studies showed that Chinese herbal medicines and traditional Chinese medicine (TCM) might regulate oxidative stress; they have already been used to treat diseases related to atherosclerosis, including stroke and myocardial infarction. This review will summarize the mechanisms of oxidative stress in atherosclerosis and discuss studies of Chinese herbal medicines and TCM preparations treating atherosclerosis, aiming to increase understanding of TCM and stimulate research for new drugs to treat diseases associated with oxidative stress.

Keywords: Chinese herbal medicines; anti-oxidant treatment; atherosclerosis; oxidative stress; traditional Chinese medicine.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Development of atherosclerotic plaques. LDL enters the arterial intima via endothelial cells expressing SR-B1 receptors in combination with DOCK4 action. LDL particles are oxidized to ox-LDL, and the monocytes entering the intima are transformed into macrophages that phagocytize ox-LDL mediated by surface SR (SR-A1, CD36). They also phagocytize other cholesterols in the intima to form foam cells. Macrophages are polarized into M1 and M2 forms. M1 macrophages release pro-inflammatory factors such as IL-6 to promote plaque progression, and oxidative stress promotes inflammatory factors. SMCs enter the intima to form fibrous caps, and oxidative stress and inflammation promote apoptosis and cell death in the plaque, leading to the accumulation of lipid and lipid cores. The continuous inflammation and oxidative stress causes the lipid nuclei to enlarge, the fibrous cap dilutes and ruptures, and platelets accumulate to form thrombi.
FIGURE 2
FIGURE 2
Oxidative stress in atherosclerosis.
See this image and copyright information in PMC

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