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Updated: Jul 23, 2025
A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats
Published on: March 1, 2022
Effects of atorvastatin in suppressing pulmonary vascular remodeling in rats with chronic obstructive pulmonary
YongHong He1, SongPing Wang1, Yuying Li1
1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou City, Sichuan Province, China.
Objective:
To investigate the effects of atorvastatin calcium on pulmonary vascular remodeling, the authors explored the regulatory mechanism of Histone Deacetylation Enzyme-2 (HDAC2) in rats with Chronic Obstructive Pulmonary Disease (COPD), and provided a new direction for drug treatment in the progression of vascular remodeling.
Methods:
Eighteen female SD rats were randomly divided into control (Group S1), COPD (Group S2), and atorvastatin calcium + COPD (Group S3) groups. A COPD rat model was established by passive smoking and intratracheal injection of Lipopolysaccharide (LPS). Haematoxylin and eosin staining and Victoria Blue + Van Gibson staining were used to observe pathological changes in the lung tissue. The pulmonary vascular inflammation score was calculated, and the degree of pulmonary vascular remodeling was evaluated. The ratio of Muscular Arteries in lung tissue (MA%), the ratio of the vessel Wall Area to the vessel total area (WA%), and the ratio of the vessel Wall Thickness to the vascular outer diameter (WT%) were measured using imaging software. The expression of HDAC2 was measured using western blotting, ELISA (Enzyme-Linked Immunosorbent Assay), and qPCR (Real-time PCR).
Results:
Compared with the control group, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling increased in rats with COPD. The WT%, WA%, and lung inflammation scores increased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissue decreased, and the level of Vascular Endothelial Growth Factor (VEGF) in the lung tissues increased (p < 0.05). Compared with the COPD group, the lung tissues from rats in the atorvastatin group had fewer inflammatory cells, and the vascular pathological changes were significantly relieved. The WT%, WA%, and lung inflammation scores decreased significantly; the expression of HDAC2 and HDAC2mRNA in the serum and lung tissues increased, and the level of VEGF in the lung tissues decreased (p < 0.05).
Conclusion:
The present study revealed that atorvastatin calcium could regulate the contents and expression of HDAC2 in serum and lung tissues and inhibit the production of VEGF, thereby regulating pulmonary vascular remodeling in a rat model with COPD.
Insights
Atorvastatin calcium treatment reduced pulmonary vascular remodeling in Chronic Obstructive Pulmonary Disease (COPD) rats by increasing Histone Deacetylation Enzyme-2 (HDAC2) expression and decreasing Vascular Endothelial Growth Factor (VEGF). This offers a new therapeutic avenue for COPD-related vascular changes.
Area of Science:
- Pulmonary Medicine
- Cardiovascular Research
- Pharmacology
Background:
- Chronic Obstructive Pulmonary Disease (COPD) is associated with pulmonary vascular remodeling.
- Histone Deacetylation Enzyme-2 (HDAC2) plays a role in vascular remodeling, but its mechanism in COPD is not fully understood.
Purpose of the Study:
- To investigate the effects of atorvastatin calcium on pulmonary vascular remodeling in a COPD rat model.
- To explore the regulatory mechanism of HDAC2 in COPD-induced vascular remodeling.
Main Methods:
- A COPD rat model was established using passive smoking and LPS instillation.
- Pulmonary vascular inflammation and remodeling were assessed using histological staining and imaging software.
- Expression levels of HDAC2 and Vascular Endothelial Growth Factor (VEGF) were measured via Western blotting, ELISA, and qPCR.
Main Results:
- COPD rats exhibited increased pulmonary vascular inflammation, remodeling (higher WT%, WA%), decreased HDAC2 expression, and increased VEGF levels.
- Atorvastatin calcium treatment significantly alleviated these pathological changes, increased HDAC2 expression, and decreased VEGF levels in COPD rats.
Conclusions:
- Atorvastatin calcium regulates pulmonary vascular remodeling in COPD by modulating HDAC2 and VEGF.
- This study provides a potential therapeutic strategy targeting HDAC2 for COPD-related vascular complications.
