Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Qi-Blood Harmony Formula ameliorates myocardial infarction in coronary atherosclerotic heart disease by reversing circRNA-mediated inhibition of angiogenesis via EIF4A3 stabilization.
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Huang Meiwen, Guo Hongai, Chen Juan, Xin Qiqi, Xie Xuena, Hu Lantian, Miao Yu, Ma Huagen, Ma Shudong, Zhu Yizhun, Yuan Rong, Cong Weihong
Аннотация
BACKGROUND: Myocardial infarction (MI) is the most severe clinical complication of coronary atherosclerotic heart disease (CHD), representing a leading cause of global morbidity and mortality. Qi-Blood Harmony Formula (QBHF), a traditional Chinese medicine, has shown clinical promise for managing MI; however, its underlying mechanisms remain to be fully elucidated.
PURPOSE: This study aimed to explore the therapeutic mechanism of QBHF against MI in the context of CHD, with a specific focus on its role in angiogenesis.
METHODS: QBHF chemical components were characterized by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry. Therapeutic efficacy was evaluated in a high-fat diet-fed ApoE-/- mouse model with left anterior descending coronary artery ligation and in a hypoxia-induced endothelial cell model. Cardiac function and angiogenesis were assessed through histological, functional, and molecular assays, with the underlying mechanisms further investigated using bioinformatics and experimental validation.
RESULTS: Chemical profiling identified 67 compounds in QBHF, with eight major constituents quantified. In atherosclerosis-myocardial infarction (AS-MI) mice, QBHF dose-dependently improved cardiac function, attenuated myocardial injury, and upregulated angiogenic markers. In vitro, QBHF enhanced hypoxia-induced proliferation, migration, and tube formation in EA.hy926 cells. Mechanistically, a specific circular RNA (hsa_circ_0003296) was found to be significantly upregulated in the peripheral blood of AS and MI patients. It directly bound to eukaryotic initiation factor 4A-III (EIF4A3) to promote its ubiquitin-mediated degradation. QBHF suppressed hsa_circ_0003296 expression, thereby preventing EIF4A3 degradation. The stabilized EIF4A3 subsequently prolonged the mRNA half-lives of vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2), thereby promoting angiogenesis.
CONCLUSIONS: These results suggest that QBHF ameliorates MI in CHD by reversing hsa_circ_0003296-mediated inhibition of angiogenesis. This process is executed through the stabilization of EIF4A3, which enhances the mRNA stability of VEGFA and VEGFR2.
PURPOSE: This study aimed to explore the therapeutic mechanism of QBHF against MI in the context of CHD, with a specific focus on its role in angiogenesis.
METHODS: QBHF chemical components were characterized by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry. Therapeutic efficacy was evaluated in a high-fat diet-fed ApoE-/- mouse model with left anterior descending coronary artery ligation and in a hypoxia-induced endothelial cell model. Cardiac function and angiogenesis were assessed through histological, functional, and molecular assays, with the underlying mechanisms further investigated using bioinformatics and experimental validation.
RESULTS: Chemical profiling identified 67 compounds in QBHF, with eight major constituents quantified. In atherosclerosis-myocardial infarction (AS-MI) mice, QBHF dose-dependently improved cardiac function, attenuated myocardial injury, and upregulated angiogenic markers. In vitro, QBHF enhanced hypoxia-induced proliferation, migration, and tube formation in EA.hy926 cells. Mechanistically, a specific circular RNA (hsa_circ_0003296) was found to be significantly upregulated in the peripheral blood of AS and MI patients. It directly bound to eukaryotic initiation factor 4A-III (EIF4A3) to promote its ubiquitin-mediated degradation. QBHF suppressed hsa_circ_0003296 expression, thereby preventing EIF4A3 degradation. The stabilized EIF4A3 subsequently prolonged the mRNA half-lives of vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2), thereby promoting angiogenesis.
CONCLUSIONS: These results suggest that QBHF ameliorates MI in CHD by reversing hsa_circ_0003296-mediated inhibition of angiogenesis. This process is executed through the stabilization of EIF4A3, which enhances the mRNA stability of VEGFA and VEGFR2.