Key result
Tongmai Yangxin pill (4.0 g/kg) alleviated myocardial no-reflow by improving cardiac structure and function, reducing ischemic areas, and decreasing cardiomyocyte injury in a rat model.
Why the study?
The effective substances and mechanisms by which Tongmai Yangxin pill alleviates myocardial no-reflow remain unclear.
Does Tongmai Yangxin pill alleviate myocardial no-reflow and improve cardiac function in a rat model?
Does Tongmai Yangxin pill alleviate myocardial no-reflow and improve cardiac function in a rat model?
Tongmai Yangxin pill demonstrates cardioprotective effects against myocardial no-reflow in a rat model, potentially mediated by GPER and HIF-1α signaling.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in animal models; leaves open translation to human no-reflow management pending clinical trials.
Context The Tongmai Yangxin pill (TMYX) has potential clinical effects on no-reflow (NR); however, the effective substances and mechanisms remain unclear.Objective This study evaluates the cardioprotective effects and molecular mechanisms of TMYX against NR.Materials and methods We used a myocardial NR rat model to confirm the effect and mechanism of action of TMYX in alleviating NR. Sprague-Dawley (SD) rats were divided into Control (Con), sham, NR, TMYX (4.0 g/kg), and sodium nitroprusside (SNP, 5.0 mg/kg), and received their treatments once a day for one week. In vitro studies in isolated coronary microvasculature of NR rats and in silico network pharmacology analyses were performed to reveal the underlying mechanisms of TMYX and determine the main components, targets, and pathways of TMYX, respectively.Results TMYX (4.0 g/kg) showed therapeutic effects on NR by improving the cardiac structure and function, reducing NR, ischemic areas, and cardiomyocyte injury, and decreasing the expression of cardiac troponin I (cTnI). Moreover, the mechanism of TMYX predicted by network pharmacology is related to the HIF-1, NF-κB, and TNF signaling pathways. In vivo, TMYX decreased the expression of MPO, NF-κB, and TNF-α and increased the expression of GPER, p-ERK, and HIF-1α. In vitro, TMYX enhanced the diastolic function of coronary microvascular cells; however, this effect was inhibited by G-15, H-89, L-NAME, ODQ and four K+ channel inhibitors.Conclusions TMYX exerts its pharmacological effects in the treatment of NR via multiple targets. However, the contribution of each pathway was not detected, and the mechanisms should be further investigated.
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Chen et al. (2023) studied Myocardial no-reflow. Tongmai Yangxin pill (TMYX) vs. Control, sham, NR, and sodium nitroprusside (SNP, 5.0 mg/kg) was evaluated on Therapeutic effects on no-reflow (cardiac structure and function, ischemic areas, cardiomyocyte injury). Tongmai Yangxin pill (4.0 g/kg) alleviated myocardial no-reflow by improving cardiac structure and function, reducing ischemic areas, and decreasing cardiomyocyte injury in a rat model.
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