title: [Endoplasmic reticulum stress and related apoptosis in the lungs of a chronic obstructive pulmonary disease rat model].
abstract: OBJECTIVE
  To study the endoplasmic reticulum stress (ERS) and the apoptosis of alveolar epithelial cells in a COPD rat model.
  
  
  METHODS
  Twenty-four Wistar rats were divided into a control group and a COPD group at random. The COPD rat model was established by intratracheal instillation of lipopolysaccharide (LPS) twice and exposure to cigarette smoke daily. The spirometry was conducted and the pathological changes were observed after the model was established. The levels of glucose regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). The protein expression of GRP78, CHOP and caspase-12 was detected by Western blot. TdT-mediated dUTP nick end labeling (TUNEL) was used to analyze alveolar epithelial cell apoptosis. Comparisons between the two groups were performed by t-test.
  
  
  RESULTS
  Significant decrease of FEV(0.3)/FVC [(60 ± 6)%] and dynamic compliance of lung (CLdyn) [(0.17 ± 0.02) cm H2O×ml(-1)×s(-1)], and increase of airway resistance [(0.64 ± 0.07) ml/cm H2O] were found in the COPD group compared with the control group [(83 ± 7)%, (0.31 ± 0.03) cm H2O×ml(-1)×s(-1), (0.32 ± 0.03) ml/cm H2O] (t = -14.532 - 11.619, P < 0.05). GRP78 mRNA and CHOP mRNA densitometry [(0.65 ± 0.07), (0.79 ± 0.06)] were significantly increased in the COPD group compared with the control group [(0.21 ± 0.04), (0.07 ± 0.04), respectively] (t = -19.102 and -32.573, P < 0.05). GRP78, CHOP, and active caspase-12 protein densitometry (0.83 ± 0.06, 0.82 ± 0.06 and 0.81 ± 0.07) were significantly increased in the COPD group compared with the control group [(0.33 ± 0.05, 0.05 ± 0.03 and 0.24 ± 0.06), respectively] (t = -40.866 - -22.070, P < 0.05). More apoptotic alveolar epithelial cells were found in the COPD group [(32.4 ± 3.7)%] than in the control group [(6.2 ± 0.9)%] (t = -23.852, P < 0.05).
  
  
  CONCLUSIONS
  ERS was triggered in the lung tissues of COPD rats, especially in the alveolar epithelial cells. Alveolar epithelial cell apoptosis was increased in the COPD group. The ERS mediated apoptosis pathway may participate in the alveolar epithelial cell apoptosis in COPD.
authors: Department of Respiratory Medicine, Xiangya Hospital of Central South University, Changsha 410008, China.
authors: Bai-mei
authors: BM
authors: He
authors: Bai-ling
authors: BL
authors: Luo
authors: Zhen-yu
authors: ZY
authors: Peng
authors: Hao
authors: H
authors: Yuan
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress; D008168:Lung / Q000378:metabolism / Q000473:pathology*; D008297:Male; D018384:Oxidative Stress; D011650:Pulmonary Alveoli / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar