Abstract
Naoxintong (NXT) is a Chinese Materia Medica standardized product extracted from 16 various kinds of Chinese traditional herbal medicines including Salvia miltiorrhiza, Angelica sinensis, Astragali Radix. Naoxintong is clinically effective in treating ischaemia heart disease. Nucleotide‐binding oligomerization domain‐Like Receptor with a Pyrin domain 3 (NLRP3) inflammasome has been critically involved in myocardial ischaemia/reperfusion (I/R) injury. Here, we have been suggested that NXT might attenuate myocardial I/R injury via suppression of NLRP3 inflammasome activation. Male C57BL6 mice were subjected to myocardial I/R injury via 45 min. coronary ligation and release for the indicated times. Naoxintong (0.7 g/kg/day) and PBS were orally administrated for 2 weeks before surgery. Cardiac function assessed by echocardiography was significantly improved in the NXT group compared to PBS group at day 2 after myocardial I/R. NLRP3 inflammasome activation is crucially involved in the initial inflammatory response after myocardial I/R injury, leading to cleaved caspase‐1, mature interleukin (IL)‐1β production, accompanying by macrophage and neutrophil infiltration. The cardioprotective effect of NXT was associated with a diminished NLRP3 inflammasome activation, decreased pro‐inflammatory macrophage (M1 macrophages) and neutrophil infiltration after myocardial I/R injury. In addition, serum levels of IL‐1β, indicators of NLRP3 inflammasome activation, were also significantly suppressed in the NXT treated group after I/R injury. Naoxintong exerts cardioprotive effects at least partly by suppression of NLRP3 inflammasome activation in this I/R injury model.
Highlights
Acute myocardial infarction (AMI) is proposed to be the major cause of death worldwide in modern society
Our results show that NXT improved cardiac function and reduced infarct area at least partly via inhibition the NLRP3 inflammasome activation, suppression of macrophage polarization towards M1 proinflammatory phenotype and neutrophil infiltration after myocardial I/ R injury
Interleukin1b can promote the increase in endothelial permeability, stimulate the release of chemokines and the expression of a number of adhesion molecules, further resulting in the recruitment of inflammatory cells such as monocytes/macrophages and neutrophils to the ischemic myocardium, amplifying the inflammatory reaction within the ischemic heart and mediates further damage [16,17,18,19,20]
Summary
Acute myocardial infarction (AMI) is proposed to be the major cause of death worldwide in modern society. Acute myocardial infarction is characterized as interruption of the blood flow due to a coronary artery occlusion. After AMI, successful reperfusion and revascularization procedures such as thrombolytic/fibrinolytic therapy and percutaneous coronary intervention may effectively reduce infarct size and improve clinical outcome. Restoration of the coronary blood flow by these procedures may lead to ‘ischaemia-reperfusion (I/R) injury’ [1]. Experimental studies in AMI animal models suggest that lethal reperfusion injury accounts for up to 50% of the final size of a myocardial infarct [2]. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine
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