| Air pollution is one of the primary risk factor in public heath. In recent years, it is known that particles less than or approximately 2.5μm in diameter (PM 2.5) are more hazardous than particles 2.5-10μm in diameter to public health. PM 2.5 may invade the bronchial, lung by inhalation, and reaches inside tissue of lung to form deposition. The long-term exposure of respiratory system to PM2.5 may give rise to bronchial inflammation. Alveolar type II epithelial cells play an important role in promoting adsorption of surface gas-liquid phospholipids, anti-infection and protection of lung tissue from damage. Some studies have showed that abnormal synthesis and metabolic of pulmonary surfactant protein B (SP-B) result in pulmonary disorder.Objective:To establish an animal model exposure to polluted dust, SP-B level in serum and lung tissue of animals is detected to provide theoretical basis of prevention and control of atmospheric pollution.Methods:78 Wistar rats (190-210g) were randomly divided into experimental groups and control groups ( experimental groups include group 1, 2, and 3,control groups include group 1, 2, and 3). Animals in experimental group are challenged with polluted dust (PM2.5) 1day, 7days and 30 days, respectively. Control rats are given to air. The SP-B levels both in pulmonary tissue and in serum are detected using immunohistochemical method, ELISA and RT-PCR.Results1. SP-B levels in BALF and in serum of rats The SP-B levels in BALF and in serum do not show significant differences between experimental group and control group (P>0.05), and there is no significant differences among the experimental groups (P>0.05).2. SP-B mRNA expression in pulmonary tissue of rats The expression levels of SP-B mRNA in experimental group 2(challenged with PM 2.5 for 7 days) is higher in comparison with in control group (P<0.01). There is no difference between experimental group 1 and group 2.3. SP-B levels in pulmonary tissue of rats SP-B levels in experimental group 3 (challenged with PM 2.5 for 30 days are higher than that in control group 3 (P<0.05), and SP-B levels in experimental group 1and 2 are lower than that in control group (P<0.01).Conclusion:1. In acute inflammation caused by air pollution, SP-B levels both in BALF and in serum exhibit no apparent changes. It is suggested that SP-B levels both in BALF and in serum can not serve as a indicator for pulmonary damage.2. Immunohistochemistry showed that SP-B levels in pulmonary tissue is lower in early inflammatory stage (1 day and 7 days) due to tissue damage.3. when animals were challenged with PM 2.5 for 7 days, the expression level of SP-B were up-regulated in comparison with control animals.4. SP-B mRNA expression may act as biological indicator of early pulmonary damage. |