摘要
Background The decrease of surfactant protein （SP） secreted by the alveolar type Ⅱ cell is one of the important causes of limiting air of pulmonary emphysema. However, the SP-A gene and protein changes in this disease are rarely studied. This study was undertaken to investigate alterations in SP-A gene activity and protein, and to explore their roles in the pathogenesis of emphysematous changes. Methods Twenty Wistar rats were divided randomly into a normal control group （n=10） and a cigarette smoking （CS） ＋ lipopolysaccharide （LPS） group （n=10）. Ultra-structural changes were observed under an electron microscope. The number of cells positive for SP-A was measured by immunohistochemistry. The mRNA expression and protein level of SP-A in the lung tissues were determined by quantitative polymerase chain reaction （qPCR） and Western blot separately. The protein level of SP-A in lavage fluid was determined by Western blot. Results The number of cells positive for SP-A of the CS＋LPS group （0.35±0.03） was lower than that of the blank control group （0.72±0.06, P 〈0.05）. The level of SP-A in the lung tissues of rats in the CS＋LPS group （0.2765±0.0890） was lower than that in the blank control group （0.6875±0.1578, P 〈0.05）. The level of SP-A in the lavage fluid of rats in the CS＋LPS group （0.8567±0.1458） was lower than that in the blank control group （1.3541±0.2475, P 〈0.05）. The lung tissues of rats in the CS＋LPS group showed an approximate increase （0.4-fold） in SP-A mRNA levels relative to β-actin mRNA （P 〈0.05）. Conclusions The changes of SP-A may be related to emphysematous changes in the lung. And cigarette smoke and LPS alter lung SP-A gene activity and protein homeostasis.
Background The decrease of surfactant protein （SP） secreted by the alveolar type Ⅱ cell is one of the important causes of limiting air of pulmonary emphysema. However, the SP-A gene and protein changes in this disease are rarely studied. This study was undertaken to investigate alterations in SP-A gene activity and protein, and to explore their roles in the pathogenesis of emphysematous changes. Methods Twenty Wistar rats were divided randomly into a normal control group （n=10） and a cigarette smoking （CS） ＋ lipopolysaccharide （LPS） group （n=10）. Ultra-structural changes were observed under an electron microscope. The number of cells positive for SP-A was measured by immunohistochemistry. The mRNA expression and protein level of SP-A in the lung tissues were determined by quantitative polymerase chain reaction （qPCR） and Western blot separately. The protein level of SP-A in lavage fluid was determined by Western blot. Results The number of cells positive for SP-A of the CS＋LPS group （0.35±0.03） was lower than that of the blank control group （0.72±0.06, P 〈0.05）. The level of SP-A in the lung tissues of rats in the CS＋LPS group （0.2765±0.0890） was lower than that in the blank control group （0.6875±0.1578, P 〈0.05）. The level of SP-A in the lavage fluid of rats in the CS＋LPS group （0.8567±0.1458） was lower than that in the blank control group （1.3541±0.2475, P 〈0.05）. The lung tissues of rats in the CS＋LPS group showed an approximate increase （0.4-fold） in SP-A mRNA levels relative to β-actin mRNA （P 〈0.05）. Conclusions The changes of SP-A may be related to emphysematous changes in the lung. And cigarette smoke and LPS alter lung SP-A gene activity and protein homeostasis.
基金
This work was supported by grants from the National Natural Science Foundation of China （No. 30500224, 3040199）.
