Abstract
At present, many patients who undergo reperfusion immediately after percutaneous coronary intervention will undergo microvascular obstruction and reduction in myocardial blood flow. This phenomenon is called “no-reflow (NR),” and there is still no effective therapy for NR. Studies showed Panax quinquefolius L. saponins (PQS) have effect on MI/R injury, while the effect and mechanism of PQS on MI/R induced NR are not clear. In this study, we established a MI/R model to investigate whether PQS decrease NR phenomenon via suppression of inflammation. We found that PQS significantly alleviated the symptoms of NR by reducing ischemia, infarction, and NR area; improving cardiac function; preventing pathological morphology changes of myocardium; depressing leukocytes’ aggregation and adhesion; and suppressing the excessive inflammation. Further study demonstrated that PQS remarkably inhibited TLR4, MyD88, p-NF-κB, and NLRP3 inflammasome-associated protein, and these effects could be reversed by LPS. These results indicated that PQS may protect NR by inhibiting the activation of NLRP3 inflammasome via TLR4/MyD88/NF-κB signaling pathway in part, suggesting that PQS exist potential in preventing NR induced by MI/R.
Highlights
Acute myocardial infarction (AMI) is the leading cause of death in the world; the prevalence and mortality rates are still on the rise
Panax quinquefolius L. saponins Repressed Serum Creatine-MB, Lactate Dehydrogenase, and cardiac troponin I Levels After MI/R
These results indicated that Panax quinquefolius L. saponins (PQS) significantly inhibited NOD-like receptor protein 3 (NLRP3) inflammasome activation and assembly, which may be related to TLR4/MyD88/ NF-κB signaling pathway
Summary
Acute myocardial infarction (AMI) is the leading cause of death in the world; the prevalence and mortality rates are still on the rise. 10%–60% patients who undergo reperfusion immediately after the initial PCI will cause microvascular occlusion and the decrease of myocardial bloodstream, and this phenomenon is called “NR” (Kalogeris et al, 2012; Cinteza, 2019; Wang et al, 2020a). It leads to the poor prognosis of patients with acute myocardial infarction, such as cardiac arrhythmia, heart failure, and cardiogenic shock. The factors associated with the establishment of NR include endothelial dysfunction, compression of capillaries by swollen myocytes, leukocyte adherence, microvascular ischemia, oxidative stress, and inflammation (Heusch, 2019; Wang et al, 2020b). Accumulating evidence indicates inflammation is considered to be a promising direction, but its underlying molecular mechanisms are not clear; there are few effective drugs
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