Abstract
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 PM2.5 (aPM2.5) particles according to the size and composition of actual PM2.5 collected in Beijing. Using these artificial particles, we created an inhalation-injury animal model. These aPM2.5 particles simulate the physical and chemical characteristics of the actual PM2.5, and inhalation of the aPM2.5 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 aPM2.5-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 aPM2.5in vitro. Treating the model rats with PD prevented the lung function decline caused by aPM2.5, and reduced the level of oxidative damage in aPM2.5-exposed rats. Moreover, PD inhibited aPM2.5-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.
Highlights
State Key Laboratory of Bioactive Substances and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100050, China. *These authors contributed to this work
APM2.5 particles were prepared with MSN as the core and three chemical species loaded into the pores of MSN
The OP of the aPM2.5 was approximately 60% that of the collected PM2.5 (Fig. 1A). These results demonstrate that the aPM2.5 were similar to the PM2.5 in terms of chemical composition, diameter, and OP
Summary
State Key Laboratory of Bioactive Substances and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100050, China. Correspondence and requests for materials should be addressed to P.-C.Z. Could ameliorate LPS-induced acute lung injury through reducing inflammation and apoptosis[16]. PD reduced septic lung injury in mice through unregulated heme oxygenase (OH-)[1] and inhibited proinflammation mediators in lung[17]. What presented below showed that PD could be a therapeutic agent to protect pulmonary impairment from air pollution
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