Tags

Type your tag names separated by a space and hit enter

Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats.
Respirology. 2009 Apr; 14(3):354-9.R

Abstract

BACKGROUND AND OBJECTIVE

The role of apoptosis in lung destruction in emphysema/COPD is increasingly being recognized. The relationship between anti-oxidants and alveolar septal cell apoptosis in COPD lungs remains to be elucidated. The aim of this study was to investigate the effects of the anti-oxidant, N-acetylcysteine (NAC), on the development of emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats.

METHODS

Sprague-Dawley rats (n = 48) were randomly assigned to normal, COPD, sham and NAC groups. The effects of treatment were assessed by measuring the levels of vascular endothelial growth factor (VEGF) in BAL fluid by ELISA, VEGF and VEGF receptor-2 (VEGFR2) protein expression by western blotting, and the apoptotic index (AI) of alveolar septal cells by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay. Histopathological evaluations (mean linear intercept (MLI), destructive index (DI)) and lung function measurements were performed.

RESULTS

FEV(0.3)/FVC and PEF were lower in the COPD group than in the normal group. MLI and DI were lower in the NAC-treated group than in the COPD or sham-treated groups. As confirmed by western blotting, the levels of VEGF in BAL fluid were higher in the NAC-treated group than in the COPD group. VEGFR2 protein expression was higher in the NAC-treated group than in the COPD group. The AI was significantly lower in the NAC-treated group than in the COPD group. There was an inverse correlation between levels of VEGF in BAL fluid and the AI of alveolar septal cells.

CONCLUSIONS

NAC attenuates lung damage, pulmonary emphysema and alveolar septal cell apoptosis by partly reversing the decrease in VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats.

Authors+Show Affiliations

Department of Respiratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19341424

Citation

Cai, Shan, et al. "Oral N-acetylcysteine Attenuates Pulmonary Emphysema and Alveolar Septal Cell Apoptosis in Smoking-induced COPD in Rats." Respirology (Carlton, Vic.), vol. 14, no. 3, 2009, pp. 354-9.
Cai S, Chen P, Zhang C, et al. Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. Respirology. 2009;14(3):354-9.
Cai, S., Chen, P., Zhang, C., Chen, J. B., & Wu, J. (2009). Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. Respirology (Carlton, Vic.), 14(3), 354-9. https://doi.org/10.1111/j.1440-1843.2009.01511.x
Cai S, et al. Oral N-acetylcysteine Attenuates Pulmonary Emphysema and Alveolar Septal Cell Apoptosis in Smoking-induced COPD in Rats. Respirology. 2009;14(3):354-9. PubMed PMID: 19341424.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oral N-acetylcysteine attenuates pulmonary emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. AU - Cai,Shan, AU - Chen,Ping, AU - Zhang,Cheng, AU - Chen,Jian-Bo, AU - Wu,Jie, PY - 2009/4/4/entrez PY - 2009/4/4/pubmed PY - 2009/7/10/medline SP - 354 EP - 9 JF - Respirology (Carlton, Vic.) JO - Respirology VL - 14 IS - 3 N2 - BACKGROUND AND OBJECTIVE: The role of apoptosis in lung destruction in emphysema/COPD is increasingly being recognized. The relationship between anti-oxidants and alveolar septal cell apoptosis in COPD lungs remains to be elucidated. The aim of this study was to investigate the effects of the anti-oxidant, N-acetylcysteine (NAC), on the development of emphysema and alveolar septal cell apoptosis in smoking-induced COPD in rats. METHODS: Sprague-Dawley rats (n = 48) were randomly assigned to normal, COPD, sham and NAC groups. The effects of treatment were assessed by measuring the levels of vascular endothelial growth factor (VEGF) in BAL fluid by ELISA, VEGF and VEGF receptor-2 (VEGFR2) protein expression by western blotting, and the apoptotic index (AI) of alveolar septal cells by terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay. Histopathological evaluations (mean linear intercept (MLI), destructive index (DI)) and lung function measurements were performed. RESULTS: FEV(0.3)/FVC and PEF were lower in the COPD group than in the normal group. MLI and DI were lower in the NAC-treated group than in the COPD or sham-treated groups. As confirmed by western blotting, the levels of VEGF in BAL fluid were higher in the NAC-treated group than in the COPD group. VEGFR2 protein expression was higher in the NAC-treated group than in the COPD group. The AI was significantly lower in the NAC-treated group than in the COPD group. There was an inverse correlation between levels of VEGF in BAL fluid and the AI of alveolar septal cells. CONCLUSIONS: NAC attenuates lung damage, pulmonary emphysema and alveolar septal cell apoptosis by partly reversing the decrease in VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats. SN - 1440-1843 UR - https://www.unboundmedicine.com/medline/citation/19341424/Oral_N_acetylcysteine_attenuates_pulmonary_emphysema_and_alveolar_septal_cell_apoptosis_in_smoking_induced_COPD_in_rats_ DB - PRIME DP - Unbound Medicine ER -