Polydatin protects the respiratory system from PM(2.5) exposure

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(2.5) collected in Beijing. Using these artificial particles, we created an inhalation-injury animal model. These aPM(2.5) particles simulate the physical and chemical characteristics of the actual PM(2.5), and inhalation of the aPM(2.5) in 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(2.5) in 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.