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Article: Role of nitric oxide in the regulation of fibrogenic factors in experimental liver fibrosis in mice

TitleRole of nitric oxide in the regulation of fibrogenic factors in experimental liver fibrosis in mice
Authors
KeywordsL-arginine
Liver fibrosis
Nitric oxide
Nitric oxide synthases
SMT
Issue Date2011
PublisherHistology and Histopathology. The Journal's web site is located at http://www.hh.um.es
Citation
Histology And Histopathology, 2011, v. 26 n. 2, p. 201-211 How to Cite?
AbstractPreviously, we have shown that an increased expression level of iNOS but a reduction in the expression of eNOS is associated with increased oxidative stress markers in CCl 4-induced experimental liver fibrosis. The present study aimed to investigate the effect of L-arginine and 5-methylisothiourea hemisulfate (SMT) in the expression of profibrogenic factors in chronic liver injury. ICR mice were treated with CCl 4 with or without treatment of L-arginine, an NO donor, or SMT, an iNOS inhibitor. The expression of matrix metalloptroteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), α-smooth muscle actin (α-SMA), tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) were investigated by RT-PCR. The activity of the MMP-2 and MMP-9 were measured by zymography. Our results showed that CCl 4treated mice showed significant up-regulation of expression of pro-fibrogenic factors, TNF-α and COX-2. Treatment with L-arginine or SMT showed a significant reduction in CCl 4-induced expression of these profibrogenic factors, TNF-α and COX-2. In conclusion, both SMT and L-arginine effectively attenuated the progression of CCl 4-induced liver fibrosis. SMT suppresses iNOS mediated NO production. However, L-arginine augments NO production. The similar effect of the two drugs on liver fibrosis indicates that there may be two distinct pathways of NOS mediated fibrogenesis in chronic liver injury by iNOS and eNOS. Our results suggest that eNOS-mediated liver fibrogenesis may play a more important role than that of iNOS in chronic liver injury. Taken together, these results support the contention that NO plays an active role in the progression of liver fibrosis and hepatocellular damage.
Persistent Identifierhttp://hdl.handle.net/10722/133315
ISSN
2015 Impact Factor: 1.875
2015 SCImago Journal Rankings: 0.805
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorLau, TYHen_HK
dc.contributor.authorNanji, AAen_HK
dc.contributor.authorTipoe, GLen_HK
dc.date.accessioned2011-05-11T08:30:36Z-
dc.date.available2011-05-11T08:30:36Z-
dc.date.issued2011en_HK
dc.identifier.citationHistology And Histopathology, 2011, v. 26 n. 2, p. 201-211en_HK
dc.identifier.issn0213-3911en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133315-
dc.description.abstractPreviously, we have shown that an increased expression level of iNOS but a reduction in the expression of eNOS is associated with increased oxidative stress markers in CCl 4-induced experimental liver fibrosis. The present study aimed to investigate the effect of L-arginine and 5-methylisothiourea hemisulfate (SMT) in the expression of profibrogenic factors in chronic liver injury. ICR mice were treated with CCl 4 with or without treatment of L-arginine, an NO donor, or SMT, an iNOS inhibitor. The expression of matrix metalloptroteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), α-smooth muscle actin (α-SMA), tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2) were investigated by RT-PCR. The activity of the MMP-2 and MMP-9 were measured by zymography. Our results showed that CCl 4treated mice showed significant up-regulation of expression of pro-fibrogenic factors, TNF-α and COX-2. Treatment with L-arginine or SMT showed a significant reduction in CCl 4-induced expression of these profibrogenic factors, TNF-α and COX-2. In conclusion, both SMT and L-arginine effectively attenuated the progression of CCl 4-induced liver fibrosis. SMT suppresses iNOS mediated NO production. However, L-arginine augments NO production. The similar effect of the two drugs on liver fibrosis indicates that there may be two distinct pathways of NOS mediated fibrogenesis in chronic liver injury by iNOS and eNOS. Our results suggest that eNOS-mediated liver fibrogenesis may play a more important role than that of iNOS in chronic liver injury. Taken together, these results support the contention that NO plays an active role in the progression of liver fibrosis and hepatocellular damage.en_HK
dc.languageengen_US
dc.publisherHistology and Histopathology. The Journal's web site is located at http://www.hh.um.esen_HK
dc.relation.ispartofHistology and Histopathologyen_HK
dc.subjectL-arginineen_HK
dc.subjectLiver fibrosisen_HK
dc.subjectNitric oxideen_HK
dc.subjectNitric oxide synthasesen_HK
dc.subjectSMTen_HK
dc.titleRole of nitric oxide in the regulation of fibrogenic factors in experimental liver fibrosis in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0213-3911&volume=26&issue=2&spage=201&epage=211&date=2011&atitle=Role+of+nitric+oxide+in+the+regulation+of+fibrogenic+factors+in+experimental+liver+fibrosis+in+mice-
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid21154234en_HK
dc.identifier.scopuseid_2-s2.0-78651305270en_HK
dc.identifier.hkuros184855en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78651305270&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue2en_HK
dc.identifier.spage201en_HK
dc.identifier.epage211en_HK
dc.identifier.isiWOS:000285238800007-
dc.publisher.placeSpainen_HK
dc.identifier.scopusauthoridLeung, TM=7202110149en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridLau, TYH=26323763000en_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK

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