Diesel vehicles-derived PM2.5 induces lung and cardiovascular injury attenuates by Securiniga suffruticosa: Involvement of NF-κB-mediated NLRP3 inflammasome activation pathway

Respiratory exposure to Particulate matter (PM), including Diesel exhaust particulate (DEP), causes oxidative stress-induced lung inflammation. Especially, fine particulate matter with an aerodynamic diameter less than 2.5 mu m (PM2.5) is a serious air pollutant associated with various health problems including cardiovascular diseases. The present study aimed to examine the inhibitory effect of Securiniga suffruticosa (S. suffruiticosa) on DEP and PM-induced lung and cardiovascular diseases. Mice inhaled DEP by using nebulizer chamber for two weeks. Treatment with S. suffruiticosa reduced the expression of C-X-C motif ligand 1/2 in bronchoalveolar lavage fluid and Muc5ac, ICAM-1, TNF-alpha, IL-6 mRNA in lung were also attenuated by S. suffruiticosa. In thoracic aorta, DEP increased CAMs, TNF-alpha and inflammasome markers such as NLRP3, Caspase-1, and ASC. However, S. suffruiticosa suppressed these levels. S. suffruiticosa inhibited PM2.5 induced production of intracellular reactive oxygen species (ROS); and inhibited the translocation of NF-kappa B p65 to the nucleus in human umbilical vein endothelial cells. Taken together, this study proved that exposure to PM2.5 induced both lung and vascular inflammation, however, S. suffruiticosa attenuated this injury via the downregulation of the NLRP3 signaling pathway. These findings suggest that S. suffruiticosa may have potential therapeutic benefit against air pollution-mediated lung and cardiovascular diseases.

Automated summary

The study investigated the protective effect of Securiniga suffruticosa against respiratory exposure to particulate matter (PM) and diesel exhaust particulate (DEP) induced lung and cardiovascular diseases. The results showed that S. suffruiticosa reduced the expression of inflammatory markers in the lungs and inhibited the NLRP3 signaling pathway. Additionally, S. suffruiticosa inhibited the production of reactive oxygen species and the translocation of NF-kappa B p65 in endothelial cells. These findings suggest that S. suffruiticosa may have therapeutic potential against air pollution-mediated lung and cardiovascular diseases.