Tuberostemonine N, an active compound isolated from Stemona tuberosa, suppresses cigarette smoke-induced sub-acute lung inflammation in mice.

OBJECTIVE

Our previous study demonstrated that a Stemona tuberosa extract had significant effects on cigarette smoking (CS)-induced lung inflammation in mice. The present study evaluated the potential of tuberostemonine N (T.N) to prevent airway inflammation and suppress airway responses in a CS-induced in vivo COPD model.

METHODS

T.N was isolated from the root of ST and analyzed using 1D and 2D NMR. The purity of T.N was accessed using HPLC-ELSD analysis. C57BL/6 mice in this study were whole-body exposed to mainstream CS or room air for 4 weeks, and T.N (1, 5 and 10 mg/kg body wt.) was administered to mice via intraperitoneal (i.p.) injection before CS exposure. The number of inflammatory cells, including neutrophils, macrophages and lymphocytes, and the amount of proinflammatory cytokines and chemokines were accessed from bronchoalveolar lavage fluid (BALF) to investigate the anti-inflammatory effects of T.N. Average alveoli size was also measured using histological analyses.

RESULTS

Cellular profiles and histopathological analyses revealed that the infiltration of peribronchial and perivascular inflammatory cells decreased significantly in the T.N-treated groups compared to the CS-exposed control group. T.N significantly inhibited the secretion of proinflammatory cytokines and chemokines in BALF and decreased alveoli size in lung tissue.

CONCLUSIONS

These data suggest that T.N exerts anti-inflammatory effects against airway inflammation, and T.N may be a novel therapeutic agent for lung diseases, such as COPD.