Atmospheric particle is one of the risk factors for respiratory disease; however, their injury mechanisms are poorly understood, and prevention methods are highly desirable. We constructed artificial PM_2.5(aPM_2.5) particles according to the size and composition of actual PM_2.5collected in Beijing. Using these artificial particles, we created an inhalation-injury animal model. These aPM_2.5particles simulate the physical and chemical characteristics of the actual PM_2.5, and inhalation of the aPM_2.5in rat results in a time-dependent change in lung suggesting a declined lung function, injury from oxidative stress and inflammation in lung. Thus, this aPM_2.5-caused injury animal model may mimic that of the pulmonary injury in human exposed to airborne particles. In addition, polydatin (PD), a resveratrol glucoside that is rich in grapes and red wine, was found to significantly decrease the oxidative potential (OP) of aPM_2.5in vitro. Treating the model rats with PD prevented the lung function decline caused by aPM_2.5, and reduced the level of oxidative damage in aPM_2.5-exposed rats. Moreover, PD inhibited aPM_2.5-induced inflammation response, as evidenced by downregulation of white blood cells in bronchoalveolar lavage fluid (BALF), inflammation-related lipids and proinflammation cytokines in lung. These results provide a practical means for self-protection against particulate air pollution.

Sensitive and convenience fatty acid HPLC-MRM quantification methods were developed based on a novel derivatization strategy.