Objective To investigate the relationship of pulmonary surfactant protein D( SP-D) with chronic obstructive pulmonary disease ( COPD) by measuring SP-D level in serum and lung tissue of rats with COPD.Methods The rat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide ( LPS) . Thirty male SD rats were randomly divided into a control group, a LPS group, and a COPD group( n =10 in each group) . The pathologic changes of lung tissue and airway were observed under light microscope by HE staining. Emphysema changes were evaluated by mean linear intercept ( MLI) of lung and mean alveolar number ( MAN) . The level of SP-D in serum was measured by enzymelinked immunosorbent assay ( ELISA) . The expression of SP-D in lung tissue was detected by Western-blot and immunohistochemistry.Results The MLI obviously increased, and MAN obviously decreased in the COPD group compared with the control group ( Plt;0.05) . There was no significant difference in the MLI and MAN between the LPS group and the control group ( Pgt;0.05) . The serum SP-D level was ( 49.59 ±2.81) ng/mL and ( 53.21±4.17) ng/mL in the LPS group and the COPD group, which was significantly higher than that in the control group [ ( 42.14±2.52) ng/mL] ( Plt;0.05) . The expression of SP-D in lung tissue was 0.56±0.01 and 0.63±0.01 in the LPS group and the COPD group, which was also obviously ber than that in the control group ( 0.39 ±0.01) ( Plt;0.05) .Meanwhile the SP-D levels in serumand lung tissue were higher in the COPD group than those in the LPS group ( Plt;0.05) . The levels of SP-D between serum and lung tissue were positively correlated in all three groups ( r=0.93, 0.94 and 0.93, respectively, Plt;0.01) .Conclusion Both the SP-D level in serum and in lung tissue increase significantly in COPD rats and correlate well each other, which suggests that SP-D may serve as a biomarker of COPD.
ObjectiveTo investigate the effects of short-time hyperoxia ventilation on lung tissue and pulmonary surfactant proteins C and D (SP-C and SP-D) in rats.MethodsSixteen male Sprague-Dawley rats were randomly divided into two groups (n=8): hyperoxia group (FiO2=0.90), air group (FiO2=0.21). Tracheal intubations were administrated after anesthesia, and rats in two groups were exposed hyperoxia or air ventilation for 4 h. At the same time, carotid artery blood gas was analyzed after 2 h and 4 h of ventilation, then oxygenation index (OI) was calculated. Four hours later, the anterior lobe of right lung was taken to observe the pathological change and the injury level was scored. The middle lobe of right lung was prepared for making tissue homogenate, and the remaining part of the lung was used to measure the wet/dry weight (W/D) ratio. The bronchoalveolar lavage fluid (BALF) was prepared in left lung. The content of SP-C and SP-D were detected in lung tissue homogenate and BALF by ELISA.ResultsComparing with hyperoxia group, the arterial partial pressure of oxygen, lung histopathology score and lung W/D ratio in air group were significantly increased (P<0.05), but OI, the content of SP-C and SP-D in lung tissue homogenate and BALF were significantly decreased (P<0.05).ConclusionHyperoxia ventilation for 4 h in rats can cause lung injury histologically, and reduce the concentration of SP-C and SP-D apparently in the lungs.