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Effect of the regulation of retinoid X receptoraI- gene expression on rat hepatic fibrosis

Aim: To study the effect of retinoid X receptor- alpha (RXR- alpha ) expression on rat hepatic fibrosis. Methods: Rat hepatic fibrosis was induced by CCl4, and the rats were randomly divided into an early-phase hepatic fibrosis group (2weeks) and a sustained hepatic fibrosis group (8weeks). They wer...

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Published in:Hepatology research 2011-05, Vol.41 (5), p.475-483
Main Authors: Wang, Zheng, Xu, Jiapeng, Zheng, Yongchao, Chen, Wei, Sun, Yongwei, Wu, Zhiyong, Luo, Meng
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container_issue 5
container_start_page 475
container_title Hepatology research
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creator Wang, Zheng
Xu, Jiapeng
Zheng, Yongchao
Chen, Wei
Sun, Yongwei
Wu, Zhiyong
Luo, Meng
description Aim: To study the effect of retinoid X receptor- alpha (RXR- alpha ) expression on rat hepatic fibrosis. Methods: Rat hepatic fibrosis was induced by CCl4, and the rats were randomly divided into an early-phase hepatic fibrosis group (2weeks) and a sustained hepatic fibrosis group (8weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR- alpha groups). A recombinant lentiviral expression vector carrying the rat RXR- alpha gene was injected into the rats to induce RXR- alpha expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR- alpha lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5&#820 8; diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. Results:In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR- alpha , alpha -smooth muscle actin ( alpha -SMA) and type I collagen (P0.05). In vitro studies revealed that expression of RXR- alpha significantly inhibited expression of alpha -SMA and type I collagen in activated HSC (P
doi_str_mv 10.1111/j.1872-034X.2011.00794.x
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Methods: Rat hepatic fibrosis was induced by CCl4, and the rats were randomly divided into an early-phase hepatic fibrosis group (2weeks) and a sustained hepatic fibrosis group (8weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR- alpha groups). A recombinant lentiviral expression vector carrying the rat RXR- alpha gene was injected into the rats to induce RXR- alpha expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR- alpha lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5&amp;#820 8; diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. Results:In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR- alpha , alpha -smooth muscle actin ( alpha -SMA) and type I collagen (P&lt;0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR- alpha showed no significant difference compared with the normal control group (P&gt;0.05). In vitro studies revealed that expression of RXR- alpha significantly inhibited expression of alpha -SMA and type I collagen in activated HSC (P&lt;0.01), as well as HSC proliferation (P&lt;0.01). Conclusion: The increased RXR- alpha gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.</description><identifier>ISSN: 1386-6346</identifier><identifier>EISSN: 1872-034X</identifier><identifier>DOI: 10.1111/j.1872-034X.2011.00794.x</identifier><language>eng</language><subject>Indexing in process</subject><ispartof>Hepatology research, 2011-05, Vol.41 (5), p.475-483</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Wang, Zheng</creatorcontrib><creatorcontrib>Xu, Jiapeng</creatorcontrib><creatorcontrib>Zheng, Yongchao</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Sun, Yongwei</creatorcontrib><creatorcontrib>Wu, Zhiyong</creatorcontrib><creatorcontrib>Luo, Meng</creatorcontrib><title>Effect of the regulation of retinoid X receptoraI- gene expression on rat hepatic fibrosis</title><title>Hepatology research</title><description>Aim: To study the effect of retinoid X receptor- alpha (RXR- alpha ) expression on rat hepatic fibrosis. Methods: Rat hepatic fibrosis was induced by CCl4, and the rats were randomly divided into an early-phase hepatic fibrosis group (2weeks) and a sustained hepatic fibrosis group (8weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR- alpha groups). A recombinant lentiviral expression vector carrying the rat RXR- alpha gene was injected into the rats to induce RXR- alpha expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR- alpha lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5&amp;#820 8; diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. Results:In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR- alpha , alpha -smooth muscle actin ( alpha -SMA) and type I collagen (P&lt;0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR- alpha showed no significant difference compared with the normal control group (P&gt;0.05). In vitro studies revealed that expression of RXR- alpha significantly inhibited expression of alpha -SMA and type I collagen in activated HSC (P&lt;0.01), as well as HSC proliferation (P&lt;0.01). 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Methods: Rat hepatic fibrosis was induced by CCl4, and the rats were randomly divided into an early-phase hepatic fibrosis group (2weeks) and a sustained hepatic fibrosis group (8weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR- alpha groups). A recombinant lentiviral expression vector carrying the rat RXR- alpha gene was injected into the rats to induce RXR- alpha expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR- alpha lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5&amp;#820 8; diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. Results:In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR- alpha , alpha -smooth muscle actin ( alpha -SMA) and type I collagen (P&lt;0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR- alpha showed no significant difference compared with the normal control group (P&gt;0.05). In vitro studies revealed that expression of RXR- alpha significantly inhibited expression of alpha -SMA and type I collagen in activated HSC (P&lt;0.01), as well as HSC proliferation (P&lt;0.01). Conclusion: The increased RXR- alpha gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.</abstract><doi>10.1111/j.1872-034X.2011.00794.x</doi></addata></record>
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title Effect of the regulation of retinoid X receptoraI- gene expression on rat hepatic fibrosis
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