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

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dc.contributor.authorLeung, Tung-Ming
dc.contributor.authorFung, Man-Lung
dc.contributor.authorLiong, Emily C.
dc.contributor.authorLau, Thomas Y.H.
dc.contributor.authorNanji, Amin A.
dc.contributor.authorTipoe, George L.
dc.date.accessioned2016-02-08T18:38:03Z
dc.date.available2016-02-08T18:38:03Z
dc.date.issued2011
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 CCl4-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 CCl4 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 RTPCR. The activity of the MMP-2 and MMP-9 were measured by zymography. Our results showed that CCl4- treated 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 CCl4-induced expression of these profibrogenic factors, TNF-α and COX-2. In conclusion, both SMT and L-arginine effectively attenuated the progression of CCl4-induced liver fibrosis. SMT suppresses iNOS mediated NO production. However, Larginine 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.es
dc.formatapplication/pdfes
dc.format.extent11es
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/47803
dc.languageenges
dc.publisherMurcia: F. Hernándezes
dc.relation.ispartofHistology and histopathology, Vol. 26, nº 2 (2011)es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectLiver fibrosises
dc.subjectNitric oxidees
dc.subject.other616 - Patología. Medicina clínica. Oncologíaes
dc.titleRole of nitric oxide in the regulation of fibrogenic factors in experimental liver fibrosis in micees
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.26, nº2 (2011)