Allicin ameliorates right heart dysfunction in rats suffering from pulmonary arterial hypertension by regulating Ca2+ communication between the sarcoplasmic reticulum and mitochondria.

Pulmonary arterial hypertension (PAH) is a chronic disease characterized by a progressive increase in pulmonary vascular pressure and resistance, which subsequently leads to right ventricular dysfunction and is the main cause of death for patients. Most drugs used for treating PAH focus on blood vessels, but no definitive treatment for PAH-induced right ventricular dysfunction is known. Recent studies have shown that allicin has a beneficial effect on PAH; however, whether allicin has a protective effect on right ventricular dysfunction caused by PAH and its specific mechanism of action are still unclear. In this study, we established a model by injecting monocrotaline. We examined the function of the pulmonary artery and right ventricle via right heart catheterization and a small animal cardiac ultrasound system, as well as HE and Masson staining. We also detected the calcium transport process and the expression of key proteins involved in calcium transport in right ventricular cells to reveal the role of the calcium communication mechanism in the treatment of PAH with right ventricular dysfunction by allicin. The results showed that allicin not only significantly improved pulmonary artery function but also improved right heart dysfunction in rats with PAH. Additionally, allicin significantly improved the calcium transport function of cardiomyocytes, increased mitochondrial ATP production, and decreased the generation of intracellular ROS.

Conclusion

Allicin protects against PAH-induced right ventricular dysfunction by regulating calcium communication between the SR and mitochondria, providing a new theoretical basis for the clinical intervention of PAH-related right heart failure.