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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 |
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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)-2,5̴ 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&#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<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>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<0.01), as well as HSC proliferation (P<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&#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<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>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<0.01), as well as HSC proliferation (P<0.01). Conclusion: The increased RXR- alpha gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.</description><subject>Indexing in process</subject><issn>1386-6346</issn><issn>1872-034X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqVi8tOwzAURK2qSPTBP9wlm7h-JSlrVAT7LqpuKje9TlwFO_V1pH4-ASH2zGZGM2cYAym4nLS5crmtVSG0OXAlpORC1C-G32ds8TfMp6y3VVFpUz2yJdFVCFkLZRbsuHMOmwzRQe4QErZjb7OP4btJmH2I_gKHKTY45JjsRwEtBgS8DwmJfsgAyWbocJieDTh_TpE8rdmDsz3h06-v2PPbbv_6Xgwp3kakfPr01GDf24BxpJOUqlRGl6XS_0C_ANnATtw</recordid><startdate>20110501</startdate><enddate>20110501</enddate><creator>Wang, Zheng</creator><creator>Xu, Jiapeng</creator><creator>Zheng, Yongchao</creator><creator>Chen, Wei</creator><creator>Sun, Yongwei</creator><creator>Wu, Zhiyong</creator><creator>Luo, Meng</creator><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20110501</creationdate><title>Effect of the regulation of retinoid X receptoraI- gene expression on rat hepatic fibrosis</title><author>Wang, Zheng ; Xu, Jiapeng ; Zheng, Yongchao ; Chen, Wei ; Sun, Yongwei ; Wu, Zhiyong ; Luo, Meng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_miscellaneous_11252435523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Indexing in process</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><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><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Hepatology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zheng</au><au>Xu, Jiapeng</au><au>Zheng, Yongchao</au><au>Chen, Wei</au><au>Sun, Yongwei</au><au>Wu, Zhiyong</au><au>Luo, Meng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of the regulation of retinoid X receptoraI- gene expression on rat hepatic fibrosis</atitle><jtitle>Hepatology research</jtitle><date>2011-05-01</date><risdate>2011</risdate><volume>41</volume><issue>5</issue><spage>475</spage><epage>483</epage><pages>475-483</pages><issn>1386-6346</issn><eissn>1872-034X</eissn><abstract>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 (P<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>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<0.01), as well as HSC proliferation (P<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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