PMID- 15854411
OWN - NLM
STAT- MEDLINE
DCOM- 20061222
LR  - 20050427
IS  - 1001-0939 (Print)
IS  - 1001-0939 (Linking)
VI  - 28
IP  - 3
DP  - 2005 Mar
TI  - [The changes of apoptosis and proliferation of pulmonary tissue in chronic 
      obstructive pulmonary disease rats].
PG  - 169-72
AB  - 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]. CONCLUSION: 
      The changes of apoptosis and proliferation of pulmonary tissue in COPD rats might 
      contribute to the pathogenesis of COPD.
FAU - Cao, Guo-qiang
AU  - Cao GQ
AD  - Department of Respiratory Medicine, Research Institute of Surgery, Daping 
      Hospital, Third Military Medical University, Chongqing 400042, China.
FAU - Qian, Gui-sheng
AU  - Qian GS
FAU - Lin, Li
AU  - Lin L
FAU - Cui, She-huai
AU  - Cui SH
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhonghua Jie He He Hu Xi Za Zhi
JT  - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal 
      of tuberculosis and respiratory diseases
JID - 8712226
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Bronchi/pathology
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Cell Proliferation
MH  - Disease Models, Animal
MH  - Lung/*pathology
MH  - Male
MH  - Pulmonary Disease, Chronic Obstructive/*pathology
MH  - Rats
MH  - Rats, Wistar
MH  - Smoking
EDAT- 2005/04/28 09:00
MHDA- 2006/12/23 09:00
CRDT- 2005/04/28 09:00
PHST- 2005/04/28 09:00 [pubmed]
PHST- 2006/12/23 09:00 [medline]
PHST- 2005/04/28 09:00 [entrez]
PST - ppublish
SO  - Zhonghua Jie He He Hu Xi Za Zhi. 2005 Mar;28(3):169-72.