Breviscapine attenuates pulmonary vascular dysfunction and inflammatory injury in a rat model of acute pulmonary embolism.

Abstract

Acute pulmonary embolism (APE) is a fatal disease characterized by pulmonary artery obstruction, leading to endothelial dysfunction, elevated pulmonary arterial pressure, right ventricular overload, and systemic inflammation. Whether breviscapine, a flavonoid glycoside with vasoprotective, anti-inflammatory, and antioxidant activities, whether protects pulmonary vascular function in APE was investigated. Male Sprague-Dawley rats were allocated at random into sham, APE, APE + low-dose breviscapine (0.2 mg/kg/day), or APE + high-dose breviscapine (1 mg/kg/day) groups. APE was induced by intravenous infusion of polystyrene microspheres, and breviscapine was administered intraperitoneally for 48 hours. Hemodynamic parameters, including mean pulmonary arterial pressure and right ventricular hypertrophy, were assessed. Lung tissues were examined histologically and immunohistochemically for endothelial markers (CD31, ICAM-1, VCAM-1) and inflammatory cytokines (IL-6, TNF-α, IL-10, MCP-1). APE caused marked pulmonary hypertension, right ventricular hypertrophy, endothelial injury, increased pro-inflammatory cytokines, and oxidative stress (p < 0.05 for all comparisons). Treatment with breviscapine, particularly with high dose, preserved endothelial structure, reduced pro-inflammatory cytokines, increased IL-10, restored endothelial markers, and corrected pulmonary hemodynamics. These results show that breviscapine maintains pulmonary vascular function and reduces inflammatory damage in APE and thus is a potential therapeutic drug.