Pulmonary artery hypertension is a refractory disease that severely affects cardiopulmonary function, mainly resulting in irreversible pulmonary vascular remodeling. Current surgical treatment of this disease is not very effective and drug treatment is targeted at relieving symptoms, improving the quality of life of patients, and preventing disease progression. The purpose of this present study was to reveal the regulatory effects of trimethoxystilbene on the serum levels of nuclear factor kappa B, interleukin-6, and tumor necrosis factor-α in a rat model of pulmonary artery hypertension and to explore the possible underlying mechanisms. Healthy Sprague Dawley rats were randomly assigned to experimental groups and treated with monocrotaline to establish the model, and we found a significant difference in the expression levels of nuclear factor kappa B, interleukin-6, and tumor necrosis factor-α between the experimental and control groups. These results suggest that trimethoxystilbene significantly reduced the inflammatory factor levels in pulmonary hypertensive rats, providing us with new potential strategies for elucidating the mechanisms of action of trimethoxystilbene in the treatment of pulmonary artery hypertension.
Reconstitution of nuclear factor kappa B activation induced by tumor necrosis factor requires membrane-associated components. Comparison with pathway activated by ceramide.
