[The changes of apoptosis and proliferation of pulmonary tissue in chronic obstructive pulmonary disease rats].
OBJECTIVE
To observe the changes of apoptosis and proliferation of pulmonary tissue cells in rats with chronic obstructive pulmonary disease (COPD).


METHODS
The rat model of COPD was established by exposure to cigarette smoking. Thirty-three Wistar rats were randomly divided into a normal control (NC) group, a smoking inhalation for 1 month (COPD-1) group and a smoking inhalation for 2 month (COPD-2) group. Pathologic changes of lung tissues and inflammatory cell differentials were studied. Immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were carried out to examine the percentage of positive cells and distribution of apoptotic cells and proliferating cells in the lung tissue.


RESULTS
Significant increases in total leukocyte numbers and neutrophils in the bronchoalveolar lavage were found in the COPD groups as compared to NC group. Two months after smoking exposure, enlargement of airspaces distal to the terminal bronchiole, destruction of alveolar walls, and loss of the alveolar unit were observed. The percentage of apoptotic cells of airway epithelium, alveolar wall cell and vascular smooth muscle cells were (36.2 +/- 8.5)%, (32.7 +/- 6.4)%, (16.1 +/- 7.2)% in COPD-1 group; (39.5 +/- 9.3)%, (37.3 +/- 7.6)%, (21.4 +/- 6.5)% in COPD-2 group; the difference being significant (all P < 0.01), as compared with NC group [(5.8 +/- 1.7)%, (6.1 +/- 2.3)%, (4.9 +/- 1.4)%]. The percentage of proliferative cells of airway epithelium, alveolar wall cell and vascular smooth muscle cells were (33.4 +/- 6.3)%, (30.1 +/- 4.6)%, (28.4 +/- 6.3)% in COPD-1 group; (35.5 +/- 9.8)%, (33.2 +/- 7.7)%, (34.5 +/- 6.7)% in COPD-2 group; the difference being significant (all P < 0.01), as compared with NC group [(7.4 +/- 2.3)%, (5.2 +/- 2.1)%, (4.4 +/- 1.8)%]. The numbers of apoptotic and proliferating cells were significantly higher in the COPD-2 group than those in the COPD-1 group (all P < 0.01). The ratio of proliferative index (PI)/apoptotic index (AI) of the pulmonary tissue cells were also different. The ratio of PI/AI of airway epithelium in COPD-1 and COPD-2 group [(0.82 +/- 0.13)%, (0.78 +/- 0.24)%] was much lower than NC group [(1.12 +/- 0.23)%, P < 0.05]; The ratio of PI/AI in small pulmonary vessels in the COPD groups [(1.55 +/- 0.25)%, (1.47 +/- 0.28)%] was significantly higher than NC group [(0.92 +/- 0.05)%, P < 0.05].


CONCLUSIONS
The changes of apoptosis and proliferation of pulmonary tissue in COPD rats might contribute to the pathogenesis of COPD.
Cao
Guo-qiang
GQ
Department of Respiratory Medicine, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Qian
Gui-sheng
GS
Lin
Li
L
Cui
She-huai
SH
D000818:Animals; D017209:Apoptosis; D001980:Bronchi / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D049109:Cell Proliferation; D004195:Disease Models, Animal; D008168:Lung / Q000473:pathology*; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D012907:Smoking