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Received Jul 27, 2017; Revised Nov 16, 2017; Accepted Dec 12, 2017
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1. Introduction
Myocardial infarction is the leading cause of death worldwide, and it is associated with sudden death and is thus a serious threat to life and health. Myocardial ischemia-reperfusion (I/R) injury is the recovery of myocardial ischemia after a short period, resulting in further deterioration of myocardial function. The pathogenesis of myocardial infarction involves many factors. I/R injury first triggers neutrophil infiltration [1, 2] and subsequently initiates the generation of a large number of oxygen-free radicals [3, 4], primes the inflammatory response including inflammasome activation [5–7], induces apoptosis [8, 9], and so on. Myocardial I/R injury is also one of the important reasons for the failure of clinical thrombolytic therapy, coronary artery bypass grafting, and heart transplantation.
Dunye Guanxinning (DG) is a class B protective traditional Chinese patent drug in the Chinese Pharmacopoeia [10]. This drug is an extract obtained from the dried rhizomes of Dioscorea zingiberensis C. H. Wright, and it is used to treat hyperlipidemia, coronary heart disease, and angina and to improve symptoms of chest tightness, palpitation, dizziness, and insomnia [10]. The fresh rhizome contains various saponins such as Huangjiangsu A, zingiberensis new saponin, deltonin, dioscin, and gracillin (Table 1) [11]. Clinical investigations have found that DG can effectively lower the blood lipid level [12], decrease angina attack frequency, shorten angina onset time, and improve endothelial function and blood rheology [13, 14]. DG also effectively reduces serum homocysteine levels in patients with ischemic heart disease [15]. The combination of DG with other traditional patent drugs has been demonstrated to decrease the incidence of angina pectoris, reinfarction, cardiac insufficiency, and platelet activation in patients with acute myocardial infarction [16]. DG effectively improves angina and myocardial infarction clinically; however, the mechanism by which it achieves this is unclear. Therefore, in this study, we used a myocardial I/R model to verify whether DG improves myocardial I/R injury by inhibiting neutrophil infiltration and inflammasome NLR family pyrin domain containing 3 (NLRP3) activity, providing a reliable basis for interpreting the mechanism of DG.
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