Shengmai Yin alleviated plaque vulnerability and ischemic myocardial damage in diesel exhaust particle-aggravated atherosclerosis with myocardial ischemia

Shuiqing Qu; Shuoqiu Deng; Ting Yang; Yuanmin Yang; Yu Zhang; Zhongyuan Zheng; Lina Chen; Yujie Li

doi:10.1016/j.ecoenv.2022.113379

Shengmai Yin alleviated plaque vulnerability and ischemic myocardial damage in diesel exhaust particle-aggravated atherosclerosis with myocardial ischemia

Ecotoxicol Environ Saf. 2022 Apr 1:234:113379. doi: 10.1016/j.ecoenv.2022.113379. Epub 2022 Mar 9.

Authors

Shuiqing Qu¹, Shuoqiu Deng¹, Ting Yang¹, Yuanmin Yang¹, Yu Zhang¹, Zhongyuan Zheng¹, Lina Chen², Yujie Li³

Affiliations

¹ Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China; Artemisinin Research Center, China Academy of Chinese Medical Sciences, Beijing, China.
² Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China; Artemisinin Research Center, China Academy of Chinese Medical Sciences, Beijing, China. Electronic address: lnchen@icmm.ac.cn.
³ Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China; Artemisinin Research Center, China Academy of Chinese Medical Sciences, Beijing, China. Electronic address: yjli@icmm.ac.cn.

PMID: 35278994
DOI: 10.1016/j.ecoenv.2022.113379

Abstract

Exposure to diesel exhaust particles (DEP) increases the risk of ischemic heart disease, especially heart attacks and ischemic/thrombotic strokes. Shengmai Yin (SMY) is a traditional Chinese medicine used to treat coronary heart disease. The aim of this study was to determine the protective role of SMY and the mechanism by which SMY affects DEP-induced cardiovascular injury. This study is expected to provide the basis for the development of an adaptive signature of SMY in the prevention of atherosclerotic cardiovascular disease and premature death from global air pollution exposure. We developed animal models of myocardial ischemia and atherosclerosis (AS) in response to DEP exposure. After SMY treatment, serum lipids returned to normal. Aortic plaque area and MMP9 expression were significantly reduced and collagen fiber expression increased after SMY treatment compared to DEP exposure alone. Thus, the risk of plaque formation and vulnerability is reduced. In addition, SMY improved left ventricular structure, morphology, function, blood flow, infarct area, myocardial damage, and ROS accumulation to varying degrees in ApoE^-/- mice. These results indicate that the use of SMY is effective, to varying degrees, for the treatment of dyslipidemia, atherosclerosis, myocardial ischemia, and oxidative stress in ApoE^-/- mice. SMY has a potential protective effect in DEP-aggravated AS in people with myocardial ischemia.

Keywords: AS development; Atherosclerosis; Cardiac dysfunction; Diesel exhaust particle; Myocardial infarction; Shengmai Yin.