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Updated: Dec 12, 2025

Author Spotlight: Investigating the Underlying Mechanisms of Right Ventricular Failure in Pulmonary Hypertension
Published on: June 14, 2024
Magnesium lithospermate B improves pulmonary artery banding induced right ventricular dysfunction by alleviating
Chen Qu1, Ying Xu2, Xilan Yang3
1Department of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China; Nanjing Medical University, Nanjing, Jiangsu, China.
Backgroud:
Magnesium lithospermate B (MLB) is a major bioactive component of Slavia miltiorrhiza, which has been widely used in heart diseases on account of its anti-inflammatory, anti-oxidative, anti-proliferative and anti-fibrotic properties. Substance P(SP) is a small molecule neuropeptide, which was secreted much more during heart failure, and has an obvious function of immune enhancement and inflammation induction. This study aimed to investigate the protective effects of MLB on pulmonary artery banding (PAB) induced right ventricular (RV) dysfunction.
Methods:
The mouse model of PAB was established. The mice were intraperitoneal (IP) injection treated with MLB (10 mg kg-1·d-1) for 4 weeks and p38 mitogen-activated protein kinase (MAPK) activator was given at the same time. Echocardiography were performed on day 28. Then the hearts were harvested, and substance P (SP), inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and cardiac fibrosis were detected. The macrophages and fibroblasts were stimulated by SP separately, and then treated with MLB as well as p38MAPK activator. The inflammatory cytokines from macrophage, the proliferation and fibrosis of cardiac fibroblasts were measured. The expression of p38MAPK proteins were confirmed by immunoblotting.
Findings:
MLB preserved RV ejection fraction (EF), FS, RV/(LV + septum), HW/BW index and blunted RV inflammation as well as fibrosis. Phosphorylated-p38 (p-p38) MAPK was up-regulated, which was partially reversed by MLB treatment. However, p38MAPK activator abolished the effects of MLB on RV dysfunction, suggesting a key role of p38MPAK pathway in the effects of MLB reversing RV dysfunction. In external experiment, MLB reversed the increase of inflammatory cytokines from macrophage, the proliferation and fibrosis of cardiac fibroblasts which was simulated by SP. In accordance with in vivo study, p38MAPK activator abolished the effects of MLB on macrophage as well as fibroblasts.
Interpretation:
MLB improves PAB induced right ventricular remodeling by alleviating inflammation via p38MAPK pathway. Thus, MLB may offer the therapeutic potential for the patients of RV dysfunction.
Insights
Magnesium lithospermate B (MLB) protects against heart failure by reducing inflammation and fibrosis through the p38MAPK pathway. This natural compound shows therapeutic potential for right ventricular dysfunction.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Magnesium lithospermate B (MLB), a component of Salvia miltiorrhiza, possesses anti-inflammatory and anti-fibrotic properties beneficial for heart disease.
- Substance P (SP) is a neuropeptide elevated in heart failure, promoting inflammation and immune responses.
Purpose of the Study:
- To investigate the protective effects of MLB against pulmonary artery banding (PAB) induced right ventricular (RV) dysfunction.
- To elucidate the role of the p38MAPK pathway in MLB's therapeutic actions on RV dysfunction.
Main Methods:
- A mouse model of PAB was established and treated with MLB and a p38MAPK activator.
- Echocardiography, biochemical assays for inflammatory cytokines and fibrosis markers, and immunoblotting were performed.
- In vitro studies assessed MLB's effects on SP-stimulated macrophages and cardiac fibroblasts.
Main Results:
- MLB treatment preserved RV function, reduced RV inflammation and fibrosis, and partially reversed p38MAPK activation.
- The p38MAPK activator negated MLB's protective effects, indicating pathway involvement.
- MLB reversed SP-induced inflammatory cytokine release, macrophage proliferation, and fibroblast fibrosis in vitro.
Conclusions:
- MLB ameliorates PAB-induced right ventricular remodeling by suppressing inflammation via the p38MAPK pathway.
- MLB demonstrates significant therapeutic potential for patients suffering from right ventricular dysfunction.
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