Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, Hunan University of Chinese Medicine, Changsha, China.
Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Pharm Biol. 2023 Dec;61(1):499-513. doi: 10.1080/13880209.2023.2184481.
The Tongmai Yangxin pill (TMYX) has potential clinical effects on no-reflow (NR); however, the effective substances and mechanisms remain unclear.
This study evaluates the cardioprotective effects and molecular mechanisms of TMYX against NR.
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. studies in isolated coronary microvasculature of NR rats and network pharmacology analyses were performed to reveal the underlying mechanisms of TMYX and determine the main components, targets, and pathways of TMYX, respectively.
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. , TMYX decreased the expression of MPO, NF-κB, and TNF-α and increased the expression of GPER, p-ERK, and HIF-1α. , 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.
TMYX exerts its pharmacological effects in the treatment of NR multiple targets. However, the contribution of each pathway was not detected, and the mechanisms should be further investigated.
通脉养心丸（TMYX）对无复流（NR）有潜在的临床疗效，但有效物质和机制尚不清楚。
本研究评价 TMYX 对 NR 的心脏保护作用及其分子机制。
我们使用心肌 NR 大鼠模型来证实 TMYX 缓解 NR 的作用和作用机制。将 Sprague-Dawley（SD）大鼠分为对照组（Con）、假手术组、NR 组、TMYX（4.0 g/kg）组和硝普钠（SNP，5.0 mg/kg）组，每天一次，连续治疗一周。进行 NR 大鼠离体冠状动脉微血管研究和网络药理学分析，分别揭示 TMYX 的潜在作用机制和确定 TMYX 的主要成分、靶点和途径。
TMYX（4.0 g/kg）通过改善心脏结构和功能、减少 NR、缺血面积和心肌细胞损伤以及降低心肌肌钙蛋白 I（cTnI）的表达，对 NR 显示出治疗作用。此外，网络药理学预测的 TMYX 作用机制与 HIF-1、NF-κB 和 TNF 信号通路有关。在离体研究中，TMYX 降低了 MPO、NF-κB 和 TNF-α的表达，增加了 GPER、p-ERK 和 HIF-1α的表达。在离体研究中，TMYX 增强了冠状动脉微血管细胞的舒张功能；然而，这种作用被 G-15、H-89、L-NAME、ODQ 和四种 K 通道抑制剂抑制。
TMYX 通过多个靶点发挥治疗 NR 的药理作用。然而，每个途径的贡献未被检测到，其机制应进一步研究。
