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Article: Characteristic comparison of three rat models induced by cigarette smoke or combined with LPS: To establish a suitable model for study of airway mucus hypersecretion in chronic obstructive pulmonary disease

TitleCharacteristic comparison of three rat models induced by cigarette smoke or combined with LPS: To establish a suitable model for study of airway mucus hypersecretion in chronic obstructive pulmonary disease
Authors
KeywordsActivator protein-1
Cigarette smoke
Histone deacetylase 2
LPS
MUC5AC
Mucus hypersecretion
Nuclear factor kappa B
Issue Date2012
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ypupt
Citation
Pulmonary Pharmacology And Therapeutics, 2012, v. 25 n. 5, p. 349-356 How to Cite?
AbstractThere is a need of in vivo COPD models for mucus hypersecretion study. The current study compared three rat models induced by cigarette smoke (CS) exposure alone or combined with pre- or post-treatment with lipopolysaccharide (LPS). Forty rats were randomly divided into the four following groups: control group, LPS + CS group (CS exposure for 4-wk combined with LPS pretreatment), CS group (CS exposure for 6-wk), CS + LPS group (CS exposure for 6-wk combined with LPS post-treatment). The results showed that both CS and CS + LPS groups had more severe pro-inflammatory cytokines secretion, inflammatory cells infiltration, and emphysema as compared to that in LPS + CS group animals. From the PAS staining sections, we found a remarkable hyperplasia of goblet-cell in epitheliums of trachea, bronchi, and bronchiole of all of three modeling groups, especially in CS and CS + LPS groups. From the western-blotting results, there were significant increase in the activities of NF-κB, AP-1, EGFR, TLR4, and MAPKs in all of three modeling groups, while HDAC2 activity was remarkably repressed in CS group only. Moreover, the expression and secretion of MUC5AC were exhibited significant increase in all of three modeling groups, which correlated well with the total transcription activity integration of NF-κB, AP-1, and HDAC2 (r = 0.946, p < 0.01). These results indicated that MUC5AC hypersecretion is consistent with activation of EGFR-AP-1/NF-κB and TLR4-AP-1/NF-κB signaling pathways, as well as repression of HDAC2 activity. Based on these results, we speculated that the 6-wk CS exposure rat model is a reliable COPD rat model, while the 6-wk CS exposure combined with LPS post-treatment rat model is a suitable COPD exacerbation model for mucus hypersecretion study. © 2012 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/153240
ISSN
2015 Impact Factor: 2.93
2015 SCImago Journal Rankings: 0.976
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNie, YCen_HK
dc.contributor.authorWu, Hen_HK
dc.contributor.authorLi, PBen_HK
dc.contributor.authorLuo, YLen_HK
dc.contributor.authorZhang, CCen_HK
dc.contributor.authorShen, JGen_HK
dc.contributor.authorSu, WWen_HK
dc.date.accessioned2012-07-16T10:01:19Z-
dc.date.available2012-07-16T10:01:19Z-
dc.date.issued2012en_HK
dc.identifier.citationPulmonary Pharmacology And Therapeutics, 2012, v. 25 n. 5, p. 349-356en_HK
dc.identifier.issn1094-5539en_HK
dc.identifier.urihttp://hdl.handle.net/10722/153240-
dc.description.abstractThere is a need of in vivo COPD models for mucus hypersecretion study. The current study compared three rat models induced by cigarette smoke (CS) exposure alone or combined with pre- or post-treatment with lipopolysaccharide (LPS). Forty rats were randomly divided into the four following groups: control group, LPS + CS group (CS exposure for 4-wk combined with LPS pretreatment), CS group (CS exposure for 6-wk), CS + LPS group (CS exposure for 6-wk combined with LPS post-treatment). The results showed that both CS and CS + LPS groups had more severe pro-inflammatory cytokines secretion, inflammatory cells infiltration, and emphysema as compared to that in LPS + CS group animals. From the PAS staining sections, we found a remarkable hyperplasia of goblet-cell in epitheliums of trachea, bronchi, and bronchiole of all of three modeling groups, especially in CS and CS + LPS groups. From the western-blotting results, there were significant increase in the activities of NF-κB, AP-1, EGFR, TLR4, and MAPKs in all of three modeling groups, while HDAC2 activity was remarkably repressed in CS group only. Moreover, the expression and secretion of MUC5AC were exhibited significant increase in all of three modeling groups, which correlated well with the total transcription activity integration of NF-κB, AP-1, and HDAC2 (r = 0.946, p < 0.01). These results indicated that MUC5AC hypersecretion is consistent with activation of EGFR-AP-1/NF-κB and TLR4-AP-1/NF-κB signaling pathways, as well as repression of HDAC2 activity. Based on these results, we speculated that the 6-wk CS exposure rat model is a reliable COPD rat model, while the 6-wk CS exposure combined with LPS post-treatment rat model is a suitable COPD exacerbation model for mucus hypersecretion study. © 2012 Elsevier Ltd.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ypupten_HK
dc.relation.ispartofPulmonary Pharmacology and Therapeuticsen_HK
dc.subjectActivator protein-1en_HK
dc.subjectCigarette smokeen_HK
dc.subjectHistone deacetylase 2en_HK
dc.subjectLPSen_HK
dc.subjectMUC5ACen_HK
dc.subjectMucus hypersecretionen_HK
dc.subjectNuclear factor kappa Ben_HK
dc.titleCharacteristic comparison of three rat models induced by cigarette smoke or combined with LPS: To establish a suitable model for study of airway mucus hypersecretion in chronic obstructive pulmonary diseaseen_HK
dc.typeArticleen_HK
dc.identifier.emailShen, JG: shenjg@hku.hken_HK
dc.identifier.authorityShen, JG=rp00487en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.pupt.2012.06.004en_HK
dc.identifier.pmid22732689-
dc.identifier.scopuseid_2-s2.0-84865988601en_HK
dc.identifier.hkuros201616en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84865988601&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue5en_HK
dc.identifier.spage349en_HK
dc.identifier.epage356en_HK
dc.identifier.isiWOS:000309374900003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridNie, YC=53865296000en_HK
dc.identifier.scopusauthoridWu, H=35222773000en_HK
dc.identifier.scopusauthoridLi, PB=10141281200en_HK
dc.identifier.scopusauthoridLuo, YL=37026466900en_HK
dc.identifier.scopusauthoridZhang, CC=55208320300en_HK
dc.identifier.scopusauthoridShen, JG=7404929947en_HK
dc.identifier.scopusauthoridSu, WW=7402010268en_HK
dc.identifier.citeulike10837170-

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