Effect of NF-κB signal pathway on mucus secretion induced by atmospheric PM2.5 in asthmatic rats.

Abstract

Exposure to PM2.5 can stimulate the mucus secretion of airway, affecting the development of bronchial asthma. NF-κB signal pathway plays an important role in inflammation and dysimmunity, what may contribute to the mucus secretion. The present study was undertaken to explore the effect of NF-κB signal pathway on mucus secretion induced by PM2.5 in rats with bronchial asthma. Fifty rats (25 males and 25 females) were divided randomly into the control group, ovalbumin asthmatic model group, asthma low-, middle- and high-dose groups (n=10, 5 males and 5 females each group). The control group, ovalbumin asthmatic model group received physiological saline; the asthma low-, middle- and high-dose groups received 1.5, 7.5 and 37.5mg/kg PM2.5 on saline, which instilled into the trachea at 2-day intervals for two doses. Lung histopathology was observed by HE staining. The mRNA levels of NF-κB family gens were detected with real time PCR. IκB-α protein expression levels were detected with Western blot. IL-1β, TNF-α and Muc5ac levels were detected by ELISA. Respiratory mucus secretion increased with increasing dose of PM2.5. Compared with healthy rats, the protein expression levels of IκB-α were significantly lower in the lung of asthmatic rats (p<0.05), while the relative mRNA expression levels of NF-κB family genes in tracheal tissue and in lung were significantly higher in the asthmatic rats (p<0.05). Serum IL-1β levels were significantly higher in the high-dose group than in the control group. Muc5ac protein levels in the trachea were higher in the high-dose compared with the low-and middle-dose groups. Short-term exposure to a high concentration of PM2.5 could up-regulate the mRNA expression levels of NF-κB family genes, activate the NF-κB signal pathway, stimulate more IL-1β and mucus secretion in rats with bronchial asthma. NF-κB signal pathway may regulate the level of IL-1β, which could influence the mucus secretion induced by PM2.5 in asthmatic rats.