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Updated: Jun 28, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Detoxification and Activating Blood Circulation Decoction Promotes Reendothelialization of Damaged Blood Vessels via
Zhiming Liu1, Guangmei Xie1, Zuwei Li2
1Jiangxi University of Chinese Medicine.
Insights
Detoxification and Activating Blood Circulation Decoction (DABCD) promotes vascular reendothelialization after angioplasty by increasing miR-126a-5p. This traditional Chinese medicine inhibits in-stent restenosis by modulating the vascular endothelial growth factor (VEGF) pathway.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- In-stent restenosis (ISR) following percutaneous coronary intervention (PCI) is a significant clinical issue.
- Promoting vascular reendothelialization is crucial for preventing endothelial proliferation and ISR.
- Understanding the molecular mechanisms underlying therapeutic interventions is essential.
Purpose of the Study:
- To elucidate the mechanism by which Detoxification and Activating Blood Circulation Decoction (DABCD) promotes vascular reendothelialization.
- To investigate the role of miRNA-126 in DABCD's effect on ISR.
- To determine DABCD's impact on the vascular endothelial growth factor (VEGF) signaling pathway.
Main Methods:
- A rat model of post-PCI restenosis was established using balloon-induced aortic injury.
- Vascular tissue and serum were collected at 14 and 28 days post-injury.
- Levels of nitric oxide (NO), endothelin-1 (ET-1), miR-126a-5p, endothelial nitric oxide synthase (eNOS), VEGF, p-Akt, and p-ERK were analyzed.
Main Results:
- DABCD treatment significantly reduced intimal hyperplasia and inflammation in the injured aorta.
- DABCD promoted vascular reendothelialization, increased nitric oxide (NO) production, and decreased ET-1 levels.
- DABCD upregulated miR-126a-5p, eNOS mRNA, and VEGF, p-Akt, and p-ERK protein expression in vascular tissue.
Conclusions:
- DABCD effectively promotes vascular reendothelialization and inhibits neointimal formation after arterial injury.
- The therapeutic effects of DABCD are mediated, in part, by the miR-126-mediated activation of the VEGF signaling pathway.
- DABCD represents a potential therapeutic strategy for preventing in-stent restenosis.
Abstract:
The occurrence of in-stent restenosis (ISR) poses a significant challenge for percutaneous coronary intervention (PCI). Thus, the promotion of vascular reendothelialization is essential to inhibit endothelial proliferation. In this study, we clarified the mechanism by which Detoxification and Activating Blood Circulation Decoction (DABCD) promotes vascular reendothelialization to avoid ISR by miRNA-126-mediated modulation of the vascular endothelial growth factor (VEGF) signaling pathway. A rat model of post-PCI restenosis was established by balloon injury. The injured aortic segment was collected 14 and 28 d after model establishment. Our findings indicate that on the 14th and 28th days following balloon injury, DABCD reduced intimal hyperplasia and inflammation and promoted vascular reendothelialization. Additionally, DABCD markedly increased nitric oxide (NO) expression and significantly decreased ET-1 production in rat serum. DABCD also increased the mRNA level of endothelial nitric oxide synthase (eNOS) and the protein expression of VEGF, p-Akt, and p-extracellular signal-regulated kinase (ERK)1/2 in vascular tissue. Unexpectedly, the expression of miR-126a-5p mRNA was significantly lower in the aortic tissue of balloon-injured rats than in the aortic tissue of control rats, and higher miR-126a-5p levels were observed in the DABCD groups. The results of this study indicated that the vascular reendothelialization effect of DABCD on arterial intimal injury is associated with the inhibition of neointimal formation and the enhancement of vascular endothelial activity. More specifically, the effects of DABCD were mediated, at least in part, through miR-126-mediated VEGF signaling pathway activation.
