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Background The decrease of suffactant 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 obsewed under an electron microscope.The number of cells positive for SP-A was measured by immunohistochemistry.The mRNA expression and protein Ievel of SP-A in the lung tissues were determined by quantitative polymerase chain reaction(qPCR)and West blot separately.The protein level of SP-A in lavage fluid was determined by West 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 controI 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 controI 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.