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[Studies on the role of colchicine in bleomycin-induced pulmonary fibrosis in rats].
Zhonghua Jie He He Hu Xi Za Zhi. 1998 Jun; 21(6):340-3.ZJ

Abstract

OBJECTIVE

It has well been known that cytokines and extracellular matrix protein (ECM) have played an important role in pulmonary fibrosis in animal model as well as in patients. The purpose of this study was to evaluate the suppressive effect of colchicine (Colc.) in bleomycin (BLM)-treated rats.

METHOD

Consecutive changes of interleukin-6(IL-6) and interleukin-8 (IL-8) released by alveolar macrophage (AM) were measured with murine B-cell hybridoma 7TD1 cells and micro membrane filter test. ECM and lipid peroxidation were observed with radioimmunoassay and biochemical assay respectively.

RESULT

(1) Colc. significantly suppressed release of IL-6 by AM from day 7 to 28 (P < 0.05). But the level of IL-6 remained higher than that of the control. On the day 1 to 3, IL-8 released by AM markedly decreased (P < 0.01) and the peak of IL-8 secretion had not appeared. (2) Colc. had no protective effects on AM lipid peroxidation injury. (3) Colc. markedly decreased the level of fibronectin (FN) by AM on day 7, 14 (P < 0.01), as well as the level of laminin (LN) in bronchoalveolar lavage fluid (BALF) on day 7 to 28. However, the level of LN remained higher than that of control. (4) Colc. lessened the collagen deposition, and the lung hydroxyproline (HYP) content decreased on day 7, 14 and 28 (P < 0.05) compared with that of the control. (5) Colc. decreased exudation of inflammatory cells in the early response, as well as the degree of fibrosis in the late stage.

CONCLUSION

Lipid peroxidation of AM might be one of the mechanisms of tissue injury and of AM activation, which increases the release of cytokines (IL-6, IL-8) and deposition of extracellular matrix proteins (FN, LN). Colc. exertes somewhat inhibitory effects on the process of pulmonary fibrosis in animal model. Factors other than AM and its cytokines might also be involved in the pathogenesis of pulmonary fibrosis in experimental rats.

Authors+Show Affiliations

Institute of Respiratory Disease, China Medical University, Shenyang 110001.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

11326889

Citation

Jiang, L, et al. "[Studies On the Role of Colchicine in Bleomycin-induced Pulmonary Fibrosis in Rats]." Zhonghua Jie He He Hu Xi Za Zhi = Zhonghua Jiehe He Huxi Zazhi = Chinese Journal of Tuberculosis and Respiratory Diseases, vol. 21, no. 6, 1998, pp. 340-3.
Jiang L, Chen B, Li Z. [Studies on the role of colchicine in bleomycin-induced pulmonary fibrosis in rats]. Zhonghua Jie He He Hu Xi Za Zhi. 1998;21(6):340-3.
Jiang, L., Chen, B., & Li, Z. (1998). [Studies on the role of colchicine in bleomycin-induced pulmonary fibrosis in rats]. Zhonghua Jie He He Hu Xi Za Zhi = Zhonghua Jiehe He Huxi Zazhi = Chinese Journal of Tuberculosis and Respiratory Diseases, 21(6), 340-3.
Jiang L, Chen B, Li Z. [Studies On the Role of Colchicine in Bleomycin-induced Pulmonary Fibrosis in Rats]. Zhonghua Jie He He Hu Xi Za Zhi. 1998;21(6):340-3. PubMed PMID: 11326889.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Studies on the role of colchicine in bleomycin-induced pulmonary fibrosis in rats]. AU - Jiang,L, AU - Chen,B, AU - Li,Z, PY - 2001/5/1/pubmed PY - 2001/6/15/medline PY - 2001/5/1/entrez SP - 340 EP - 3 JF - Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases JO - Zhonghua Jie He He Hu Xi Za Zhi VL - 21 IS - 6 N2 - OBJECTIVE: It has well been known that cytokines and extracellular matrix protein (ECM) have played an important role in pulmonary fibrosis in animal model as well as in patients. The purpose of this study was to evaluate the suppressive effect of colchicine (Colc.) in bleomycin (BLM)-treated rats. METHOD: Consecutive changes of interleukin-6(IL-6) and interleukin-8 (IL-8) released by alveolar macrophage (AM) were measured with murine B-cell hybridoma 7TD1 cells and micro membrane filter test. ECM and lipid peroxidation were observed with radioimmunoassay and biochemical assay respectively. RESULT: (1) Colc. significantly suppressed release of IL-6 by AM from day 7 to 28 (P < 0.05). But the level of IL-6 remained higher than that of the control. On the day 1 to 3, IL-8 released by AM markedly decreased (P < 0.01) and the peak of IL-8 secretion had not appeared. (2) Colc. had no protective effects on AM lipid peroxidation injury. (3) Colc. markedly decreased the level of fibronectin (FN) by AM on day 7, 14 (P < 0.01), as well as the level of laminin (LN) in bronchoalveolar lavage fluid (BALF) on day 7 to 28. However, the level of LN remained higher than that of control. (4) Colc. lessened the collagen deposition, and the lung hydroxyproline (HYP) content decreased on day 7, 14 and 28 (P < 0.05) compared with that of the control. (5) Colc. decreased exudation of inflammatory cells in the early response, as well as the degree of fibrosis in the late stage. CONCLUSION: Lipid peroxidation of AM might be one of the mechanisms of tissue injury and of AM activation, which increases the release of cytokines (IL-6, IL-8) and deposition of extracellular matrix proteins (FN, LN). Colc. exertes somewhat inhibitory effects on the process of pulmonary fibrosis in animal model. Factors other than AM and its cytokines might also be involved in the pathogenesis of pulmonary fibrosis in experimental rats. SN - 1001-0939 UR - https://www.unboundmedicine.com/medline/citation/11326889/[Studies_on_the_role_of_colchicine_in_bleomycin_induced_pulmonary_fibrosis_in_rats]_ L2 - https://medlineplus.gov/pulmonaryfibrosis.html DB - PRIME DP - Unbound Medicine ER -