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Article: Inhibition of hepatic stellate cell activation following Yinchenhao decoction administration to dimethylnitrosamine-treated rats

TitleInhibition of hepatic stellate cell activation following Yinchenhao decoction administration to dimethylnitrosamine-treated rats
Authors
KeywordsAntifibrogenic
Hepatic stellate cells
Liver fibrosis
Yinchenhao decoction
Issue Date2008
PublisherBlackwell Publishing Ltd
Citation
Hepatology Research, 2008, v. 38 n. 9, p. 919-929 How to Cite?
AbstractAim: In an effort to investigate the mechanism by which Yinchenhao decoction (YCHD) acts on liver injury, we investigated the potential antifibrogenic effects of YCHD in an experimental liver fibrosis rat model, with special focus on the mechanisms inhibiting the activation and promoting apoptosis of hepatic stellate cells (HSC). Methods: The rats were initially randomized into two groups: the control (n = 10) and dimethylnitrosamine-treated (DMN; n = 30) groups. DMN (10 mg/kg body weight) was administered intraperitoneally to the DMN-treated rats for three consecutive days each week. At the end of the second week, three rats from the control and six rats from the DMN-treated groups were killed for the fibrosis development assessment. The remaining DMN rats were further randomized into two groups: the DMN-water group (n = 12) and the DMN-YCHD group (n = 12). Both groups continued to receive weekly DMN treatment for another 2 weeks in addition to daily administration of either water or YCHD, which were given intragastrically at a dose of 0.418 g/100 g body weight. Results: Hepatic hydroxyproline content decreased and had improved histopathology in the DMN-YCHD rats. Compared to the DMN group, α-smooth muscle actin (SMA) and CD68 expression in the DMN-YCHD group was reduced significantly; however, α-SMA-positive HSC apoptosis was not observed by confocal microscopy; Fibrogenic proteins (tissue inhibitor matrix proteinases-1 and 2 and matrix metalloproteinase [MMP]-2/14) and cytokines (tumor necrosis factor-α and transforming growth factor-β1) were decreased; MMP-9 was significantly upregulated. Conclusion: Yinchenhao administration attenuates liver fibrosis at least in part by inhibiting HSC activation directly, rather than promoting cell apoptosis of activated HSC, and the suppressive activation of Kupffer cells. © 2008 The Japan Society of Hepatology.
Persistent Identifierhttp://hdl.handle.net/10722/60725
ISSN
2015 Impact Factor: 2.208
2015 SCImago Journal Rankings: 0.782
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Cen_HK
dc.contributor.authorSun, Men_HK
dc.contributor.authorYan, Xen_HK
dc.contributor.authorHan, Len_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorLiu, Cen_HK
dc.contributor.authorElNezami, Hen_HK
dc.contributor.authorLiu, Pen_HK
dc.date.accessioned2010-05-31T04:17:13Z-
dc.date.available2010-05-31T04:17:13Z-
dc.date.issued2008en_HK
dc.identifier.citationHepatology Research, 2008, v. 38 n. 9, p. 919-929en_HK
dc.identifier.issn1386-6346en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60725-
dc.description.abstractAim: In an effort to investigate the mechanism by which Yinchenhao decoction (YCHD) acts on liver injury, we investigated the potential antifibrogenic effects of YCHD in an experimental liver fibrosis rat model, with special focus on the mechanisms inhibiting the activation and promoting apoptosis of hepatic stellate cells (HSC). Methods: The rats were initially randomized into two groups: the control (n = 10) and dimethylnitrosamine-treated (DMN; n = 30) groups. DMN (10 mg/kg body weight) was administered intraperitoneally to the DMN-treated rats for three consecutive days each week. At the end of the second week, three rats from the control and six rats from the DMN-treated groups were killed for the fibrosis development assessment. The remaining DMN rats were further randomized into two groups: the DMN-water group (n = 12) and the DMN-YCHD group (n = 12). Both groups continued to receive weekly DMN treatment for another 2 weeks in addition to daily administration of either water or YCHD, which were given intragastrically at a dose of 0.418 g/100 g body weight. Results: Hepatic hydroxyproline content decreased and had improved histopathology in the DMN-YCHD rats. Compared to the DMN group, α-smooth muscle actin (SMA) and CD68 expression in the DMN-YCHD group was reduced significantly; however, α-SMA-positive HSC apoptosis was not observed by confocal microscopy; Fibrogenic proteins (tissue inhibitor matrix proteinases-1 and 2 and matrix metalloproteinase [MMP]-2/14) and cytokines (tumor necrosis factor-α and transforming growth factor-β1) were decreased; MMP-9 was significantly upregulated. Conclusion: Yinchenhao administration attenuates liver fibrosis at least in part by inhibiting HSC activation directly, rather than promoting cell apoptosis of activated HSC, and the suppressive activation of Kupffer cells. © 2008 The Japan Society of Hepatology.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltden_HK
dc.relation.ispartofHepatology Researchen_HK
dc.rightsHepatology Research . Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectAntifibrogenicen_HK
dc.subjectHepatic stellate cellsen_HK
dc.subjectLiver fibrosisen_HK
dc.subjectYinchenhao decoctionen_HK
dc.titleInhibition of hepatic stellate cell activation following Yinchenhao decoction administration to dimethylnitrosamine-treated ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1386-6346&volume=38&spage=919&epage=29&date=2008&atitle=Inhibition+of+hepatic+stellate+cell+activation+following+Yinchenhao+decoction+administration+to+dimethylnitrosamine-treated+rats.en_HK
dc.identifier.emailElNezami, H: elnezami@hkucc.hku.hken_HK
dc.identifier.authorityElNezami, H=rp00694en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1872-034X.2008.00346.xen_HK
dc.identifier.scopuseid_2-s2.0-48949089205en_HK
dc.identifier.hkuros151554en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48949089205&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume38en_HK
dc.identifier.issue9en_HK
dc.identifier.spage919en_HK
dc.identifier.epage929en_HK
dc.identifier.isiWOS:000258208700009-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridLiu, C=36063265000en_HK
dc.identifier.scopusauthoridSun, M=8269150600en_HK
dc.identifier.scopusauthoridYan, X=24504531100en_HK
dc.identifier.scopusauthoridHan, L=37019828400en_HK
dc.identifier.scopusauthoridZhang, Y=35313266800en_HK
dc.identifier.scopusauthoridLiu, C=36064322500en_HK
dc.identifier.scopusauthoridElNezami, H=6603690577en_HK
dc.identifier.scopusauthoridLiu, P=36065603800en_HK

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