Keywords
Myocardial angiogenesis
PDGF/IGF-1/VEGF
Zhuang Medicine Longzuan Tongbi Decoction
Submitted : 2026-06-10
Accepted : 2026-06-25
Published : 2026-07-10
Abstract
Objective: To investigate the effects of Zhuang Medicine Longzuan Tongbi Decoction on left ventricular remodeling in rats after myocardial infarction (MI), and to explain its underlying mechanism based on expressions of PDGF, IGF‑1, VEGF and related inflammatory factors. Methods: A total of 120 SD rats were randomly divided into a sham operation group, a model group, a positive control (Shexiang Baoxin Pill) group, as well as low-, medium-, and high-dose groups of Longzuan Tongbi Decoction. The MI model was established by ligation of the left anterior descending coronary artery. Postoperatively, gavage administration was performed once daily for 6 consecutive weeks. At the end of the experiment, the infarct size and microvessel density in myocardial tissues were measured; the expression levels of PDGF, IGF‑1, VEGF, IL‑1β and IL‑6 in myocardium were detected, and the serum contents of IL‑1β and IL‑6 were determined. Results: Compared with the model group, all dosage groups of Longzuan Tongbi Decoction significantly reduced myocardial infarct size, elevated the number and density of microvessels in myocardial tissue, upregulated the protein expressions of PDGF, IGF‑1 and VEGF in myocardium, and downregulated the levels of IL‑1β and IL‑6 in myocardial tissue and serum (P < 0.05). In terms of promoting angiogenesis and regulating related cytokines, the medium‑ and high‑dose groups of Longzuan Tongbi Decoction exhibited superior efficacy to the Shexiang Baoxin Pill group (P < 0.05), with an overall dose‑dependent effect. Conclusion: Zhuang Medicine Longzuan Tongbi Decoction may exert synergistic multi‑target effects to upregulate the expression of pro‑angiogenic factors and suppress inflammatory responses, thereby facilitating myocardial angiogenesis and ameliorating left ventricular remodeling. Its underlying mechanism is closely associated with the regulation of angiogenesis‑ and inflammation‑related signaling pathways.
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