Department of Analytical Biosciences, Leiden Academic Center for Drug Research, Leiden University, Einsteinweg 55, 2333 CC, Leiden, The Netherlands.
Hebei Medical University, Shijiazhuang, Hebei, 050017, P.R., China.
Sci Rep. 2018 Feb 27;8(1):3688. doi: 10.1038/s41598-018-22074-6.
The Chinese medicine Qiliqiangxin (QL) has been shown to have a protective role in heart failure. Here, we explore the underlying working mechanism of the key therapeutic component in QL using a rat model of heart failure. Heart failure after myocardial infarction was induced surgically and confirmed using echocardiography; a separate group of rats underwent sham surgery. The rats with heart failure were randomly assigned to receive QL, the angiotensin-converting enzyme inhibitor benazepril, or placebo groups. Blood samples were collected from the rats at four time points for up to 8 weeks and used for biochemical analysis and mass spectrometry‒based metabolomics profiling. In total, we measured nine well-known biochemical parameters of heart failure and 147 metabolites. In the rats with heart failure, QL significantly improved these biochemical parameters and metabolomics profiles, significantly increasing the cardioprotective parameter angiopoietin-like 4 and significantly lowering inflammation-related oxylipins and lysophosphatidic acids compared to benazepril. Mechanistically, QL may improve outcome in heart failure by controlling inflammatory process and cardiac hypertrophy. Clinical studies should be designed in order to investigate these putative mechanisms in patients.
中药芪苈强心（QL）已被证明在心力衰竭中具有保护作用。在这里，我们使用心力衰竭大鼠模型探索 QL 中关键治疗成分的潜在作用机制。通过手术诱导心肌梗死后心力衰竭，并通过超声心动图确认；另一组大鼠接受假手术。心力衰竭大鼠被随机分配到接受 QL、血管紧张素转换酶抑制剂贝那普利或安慰剂组。在 8 周的时间内，从大鼠身上采集 4 个时间点的血液样本，用于生化分析和基于质谱的代谢组学分析。总共测量了心力衰竭的 9 个已知生化参数和 147 种代谢物。在心力衰竭大鼠中，QL 显著改善了这些生化参数和代谢组学图谱，与贝那普利相比，显著增加了心脏保护参数血管生成素样 4，显著降低了炎症相关的氧化脂类和溶血磷脂酸。从机制上讲，QL 可能通过控制炎症过程和心脏肥大来改善心力衰竭的预后。应设计临床研究以在患者中研究这些潜在机制。
