Protective Effects of Colchicine in an Experimental Rat Endometriosis Model: Histopathological Evaluation and Assessment of TNF-α Levels
Objective: Endometriosis is an estrogen-dependent chronic inflammatory disease observed in reproductive period. The aim of the present study is to assess the efficacy of colchicine, widely used to treat many inflammatory diseases, in an experimental rat endometriosis model. Study Design: Experimenta...
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| Veröffentlicht in: | Reproductive sciences (Thousand Oaks, Calif.) Calif.), 2015-02, Vol.22 (2), p.258-263 |
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| creator | Kurt, Raziye Keskin Pinar, Neslihan Karateke, Atilla Okyay, Ayşe Güler Silfeler, Dilek Benk Albayrak, Aynur Özdemir, Seyda Hakverdi, Ali Ulvi |
| description | Objective:
Endometriosis is an estrogen-dependent chronic inflammatory disease observed in reproductive period. The aim of the present study is to assess the efficacy of colchicine, widely used to treat many inflammatory diseases, in an experimental rat endometriosis model.
Study Design:
Experimental endometriosis was constituted with implantation of autogenous endometrial tissue. Rats were divided randomly into 2 groups as colchicine group (n = 8) and control group (n =8). Although oral 0.1 mg/kg colchicine was administered 4 weeks to the colchicine group, the same amount of saline solution was administered to the control group. Before and after 30 days of treatment period, peritoneal and tissue tumor necrosis factor α (TNF-α), the volumes and histopathological properties of the implants were evaluated.
Results:
Although the implant volume decreased significantly in the colchicine group (89.2 ± 13.4 mm3 to 35.2 ± 4.5 mm3, P < .05), the implant volume increased in the control group (85.1 ± 14.2 mm3 to 110.3 ± 10.5 mm3, P < .05). When compared to the control group, the colchicine group had significantly lower histopathologic sores (1.4 ± 0.2 vs 2.6 ± 0.4, P < .001). Although peritoneal fluid TNF-α levels were significantly decreased in the colchicine group (45.2 ± 5.3 pg/mL vs 12.1 ± 5.2 pg/mL, P < .001), the peritoneal fluid TNF-α levels were significantly increased in the control group after the treatment (44.2 ± 3.5 pg/mL vs 61.3 ± 12.2 pg/mL; P < .001). Tissue TNF-α levels were significantly lower in the colchicine group when compared to the control group (45.4 ± 8.6 pg/mL vs 71.3 ± 11.2 pg/mL; P < .001).
Conclusion:
Colchicine resulted in regression of endometrial implant volumes in experimental rat endometriosis model and decreased peritoneal and tissue TNF-α levels. |
| doi_str_mv | 10.1177/1933719114542029 |
| format | Article |
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Endometriosis is an estrogen-dependent chronic inflammatory disease observed in reproductive period. The aim of the present study is to assess the efficacy of colchicine, widely used to treat many inflammatory diseases, in an experimental rat endometriosis model.
Study Design:
Experimental endometriosis was constituted with implantation of autogenous endometrial tissue. Rats were divided randomly into 2 groups as colchicine group (n = 8) and control group (n =8). Although oral 0.1 mg/kg colchicine was administered 4 weeks to the colchicine group, the same amount of saline solution was administered to the control group. Before and after 30 days of treatment period, peritoneal and tissue tumor necrosis factor α (TNF-α), the volumes and histopathological properties of the implants were evaluated.
Results:
Although the implant volume decreased significantly in the colchicine group (89.2 ± 13.4 mm3 to 35.2 ± 4.5 mm3, P < .05), the implant volume increased in the control group (85.1 ± 14.2 mm3 to 110.3 ± 10.5 mm3, P < .05). When compared to the control group, the colchicine group had significantly lower histopathologic sores (1.4 ± 0.2 vs 2.6 ± 0.4, P < .001). Although peritoneal fluid TNF-α levels were significantly decreased in the colchicine group (45.2 ± 5.3 pg/mL vs 12.1 ± 5.2 pg/mL, P < .001), the peritoneal fluid TNF-α levels were significantly increased in the control group after the treatment (44.2 ± 3.5 pg/mL vs 61.3 ± 12.2 pg/mL; P < .001). Tissue TNF-α levels were significantly lower in the colchicine group when compared to the control group (45.4 ± 8.6 pg/mL vs 71.3 ± 11.2 pg/mL; P < .001).
Conclusion:
Colchicine resulted in regression of endometrial implant volumes in experimental rat endometriosis model and decreased peritoneal and tissue TNF-α levels.]]></description><identifier>ISSN: 1933-7191</identifier><identifier>EISSN: 1933-7205</identifier><identifier>DOI: 10.1177/1933719114542029</identifier><identifier>PMID: 25049286</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Ascitic Fluid - immunology ; Ascitic Fluid - metabolism ; Cell Proliferation - drug effects ; Colchicine - pharmacology ; Cytoprotection ; Disease Models, Animal ; Down-Regulation ; Embryology ; Endometriosis - immunology ; Endometriosis - metabolism ; Endometriosis - pathology ; Endometriosis - prevention & control ; Endometrium - drug effects ; Endometrium - immunology ; Endometrium - metabolism ; Endometrium - pathology ; Endometrium - transplantation ; Female ; Medicine & Public Health ; Obstetrics/Perinatology/Midwifery ; Original Article ; Rats, Wistar ; Reproductive Medicine ; Time Factors ; Tumor Necrosis Factor-alpha - blood ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Reproductive sciences (Thousand Oaks, Calif.), 2015-02, Vol.22 (2), p.258-263</ispartof><rights>The Author(s) 2014</rights><rights>Society for Reproductive Investigation 2015</rights><rights>The Author(s) 2014.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c379t-3aad487bd63b9340b19c43af652b89744accf56030f8b7d3cc5d7c4980fd12d43</citedby><cites>FETCH-LOGICAL-c379t-3aad487bd63b9340b19c43af652b89744accf56030f8b7d3cc5d7c4980fd12d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/1933719114542029$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/1933719114542029$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>315,782,786,21828,27933,27934,41497,42566,43630,43631,51328</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25049286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kurt, Raziye Keskin</creatorcontrib><creatorcontrib>Pinar, Neslihan</creatorcontrib><creatorcontrib>Karateke, Atilla</creatorcontrib><creatorcontrib>Okyay, Ayşe Güler</creatorcontrib><creatorcontrib>Silfeler, Dilek Benk</creatorcontrib><creatorcontrib>Albayrak, Aynur</creatorcontrib><creatorcontrib>Özdemir, Seyda</creatorcontrib><creatorcontrib>Hakverdi, Ali Ulvi</creatorcontrib><title>Protective Effects of Colchicine in an Experimental Rat Endometriosis Model: Histopathological Evaluation and Assessment of TNF-α Levels</title><title>Reproductive sciences (Thousand Oaks, Calif.)</title><addtitle>Reprod. Sci</addtitle><addtitle>Reprod Sci</addtitle><description><![CDATA[Objective:
Endometriosis is an estrogen-dependent chronic inflammatory disease observed in reproductive period. The aim of the present study is to assess the efficacy of colchicine, widely used to treat many inflammatory diseases, in an experimental rat endometriosis model.
Study Design:
Experimental endometriosis was constituted with implantation of autogenous endometrial tissue. Rats were divided randomly into 2 groups as colchicine group (n = 8) and control group (n =8). Although oral 0.1 mg/kg colchicine was administered 4 weeks to the colchicine group, the same amount of saline solution was administered to the control group. Before and after 30 days of treatment period, peritoneal and tissue tumor necrosis factor α (TNF-α), the volumes and histopathological properties of the implants were evaluated.
Results:
Although the implant volume decreased significantly in the colchicine group (89.2 ± 13.4 mm3 to 35.2 ± 4.5 mm3, P < .05), the implant volume increased in the control group (85.1 ± 14.2 mm3 to 110.3 ± 10.5 mm3, P < .05). When compared to the control group, the colchicine group had significantly lower histopathologic sores (1.4 ± 0.2 vs 2.6 ± 0.4, P < .001). Although peritoneal fluid TNF-α levels were significantly decreased in the colchicine group (45.2 ± 5.3 pg/mL vs 12.1 ± 5.2 pg/mL, P < .001), the peritoneal fluid TNF-α levels were significantly increased in the control group after the treatment (44.2 ± 3.5 pg/mL vs 61.3 ± 12.2 pg/mL; P < .001). Tissue TNF-α levels were significantly lower in the colchicine group when compared to the control group (45.4 ± 8.6 pg/mL vs 71.3 ± 11.2 pg/mL; P < .001).
Conclusion:
Colchicine resulted in regression of endometrial implant volumes in experimental rat endometriosis model and decreased peritoneal and tissue TNF-α levels.]]></description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Ascitic Fluid - immunology</subject><subject>Ascitic Fluid - metabolism</subject><subject>Cell Proliferation - drug effects</subject><subject>Colchicine - pharmacology</subject><subject>Cytoprotection</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Embryology</subject><subject>Endometriosis - immunology</subject><subject>Endometriosis - metabolism</subject><subject>Endometriosis - pathology</subject><subject>Endometriosis - prevention & control</subject><subject>Endometrium - drug effects</subject><subject>Endometrium - immunology</subject><subject>Endometrium - metabolism</subject><subject>Endometrium - pathology</subject><subject>Endometrium - transplantation</subject><subject>Female</subject><subject>Medicine & Public Health</subject><subject>Obstetrics/Perinatology/Midwifery</subject><subject>Original Article</subject><subject>Rats, Wistar</subject><subject>Reproductive Medicine</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1933-7191</issn><issn>1933-7205</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkDtPwzAUhS0EoqWwMyGPLAE7tuN4RFV5iCIQgjly_CiukrjYCYJ_j6u2DAyI6R7d-50j3QPAKUYXGHN-iQUhHAuMKaM5ysUeGK9XGc8R29_pdB-BoxiXCDEq8vIQjHKG1qoYg_un4Hujevdh4MzapCL0Fk59o96ccp2BroOyg7PPlQmuNV0vG_gsezjrtG9NH5yPLsIHr01zDA6sbKI52c4JeL2evUxvs_njzd30ap4pwkWfESk1LXmtC1ILQlGNhaJE2oLldSk4pVIpywpEkC1rrolSTHNFRYmsxrmmZALON7mr4N8HE_uqdVGZppGd8UOscEEZ54ISklC0QVXwMQZjq1X6QoavCqNqXWH1u8JkOdumD3Vr9I9h11kC8AaI6dQtTKiWfghd-viv0GzrkQvzD_4bKW-G4w</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Kurt, Raziye Keskin</creator><creator>Pinar, Neslihan</creator><creator>Karateke, Atilla</creator><creator>Okyay, Ayşe Güler</creator><creator>Silfeler, Dilek Benk</creator><creator>Albayrak, Aynur</creator><creator>Özdemir, Seyda</creator><creator>Hakverdi, Ali Ulvi</creator><general>SAGE Publications</general><general>Springer International Publishing</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20150201</creationdate><title>Protective Effects of Colchicine in an Experimental Rat Endometriosis Model</title><author>Kurt, Raziye Keskin ; Pinar, Neslihan ; Karateke, Atilla ; Okyay, Ayşe Güler ; Silfeler, Dilek Benk ; Albayrak, Aynur ; Özdemir, Seyda ; Hakverdi, Ali Ulvi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c379t-3aad487bd63b9340b19c43af652b89744accf56030f8b7d3cc5d7c4980fd12d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Ascitic Fluid - immunology</topic><topic>Ascitic Fluid - metabolism</topic><topic>Cell Proliferation - drug effects</topic><topic>Colchicine - pharmacology</topic><topic>Cytoprotection</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Embryology</topic><topic>Endometriosis - immunology</topic><topic>Endometriosis - metabolism</topic><topic>Endometriosis - pathology</topic><topic>Endometriosis - prevention & control</topic><topic>Endometrium - drug effects</topic><topic>Endometrium - immunology</topic><topic>Endometrium - metabolism</topic><topic>Endometrium - pathology</topic><topic>Endometrium - transplantation</topic><topic>Female</topic><topic>Medicine & Public Health</topic><topic>Obstetrics/Perinatology/Midwifery</topic><topic>Original Article</topic><topic>Rats, Wistar</topic><topic>Reproductive Medicine</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kurt, Raziye Keskin</creatorcontrib><creatorcontrib>Pinar, Neslihan</creatorcontrib><creatorcontrib>Karateke, Atilla</creatorcontrib><creatorcontrib>Okyay, Ayşe Güler</creatorcontrib><creatorcontrib>Silfeler, Dilek Benk</creatorcontrib><creatorcontrib>Albayrak, Aynur</creatorcontrib><creatorcontrib>Özdemir, Seyda</creatorcontrib><creatorcontrib>Hakverdi, Ali Ulvi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Reproductive sciences (Thousand Oaks, Calif.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kurt, Raziye Keskin</au><au>Pinar, Neslihan</au><au>Karateke, Atilla</au><au>Okyay, Ayşe Güler</au><au>Silfeler, Dilek Benk</au><au>Albayrak, Aynur</au><au>Özdemir, Seyda</au><au>Hakverdi, Ali Ulvi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effects of Colchicine in an Experimental Rat Endometriosis Model: Histopathological Evaluation and Assessment of TNF-α Levels</atitle><jtitle>Reproductive sciences (Thousand Oaks, Calif.)</jtitle><stitle>Reprod. Sci</stitle><addtitle>Reprod Sci</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>22</volume><issue>2</issue><spage>258</spage><epage>263</epage><pages>258-263</pages><issn>1933-7191</issn><eissn>1933-7205</eissn><abstract><![CDATA[Objective:
Endometriosis is an estrogen-dependent chronic inflammatory disease observed in reproductive period. The aim of the present study is to assess the efficacy of colchicine, widely used to treat many inflammatory diseases, in an experimental rat endometriosis model.
Study Design:
Experimental endometriosis was constituted with implantation of autogenous endometrial tissue. Rats were divided randomly into 2 groups as colchicine group (n = 8) and control group (n =8). Although oral 0.1 mg/kg colchicine was administered 4 weeks to the colchicine group, the same amount of saline solution was administered to the control group. Before and after 30 days of treatment period, peritoneal and tissue tumor necrosis factor α (TNF-α), the volumes and histopathological properties of the implants were evaluated.
Results:
Although the implant volume decreased significantly in the colchicine group (89.2 ± 13.4 mm3 to 35.2 ± 4.5 mm3, P < .05), the implant volume increased in the control group (85.1 ± 14.2 mm3 to 110.3 ± 10.5 mm3, P < .05). When compared to the control group, the colchicine group had significantly lower histopathologic sores (1.4 ± 0.2 vs 2.6 ± 0.4, P < .001). Although peritoneal fluid TNF-α levels were significantly decreased in the colchicine group (45.2 ± 5.3 pg/mL vs 12.1 ± 5.2 pg/mL, P < .001), the peritoneal fluid TNF-α levels were significantly increased in the control group after the treatment (44.2 ± 3.5 pg/mL vs 61.3 ± 12.2 pg/mL; P < .001). Tissue TNF-α levels were significantly lower in the colchicine group when compared to the control group (45.4 ± 8.6 pg/mL vs 71.3 ± 11.2 pg/mL; P < .001).
Conclusion:
Colchicine resulted in regression of endometrial implant volumes in experimental rat endometriosis model and decreased peritoneal and tissue TNF-α levels.]]></abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>25049286</pmid><doi>10.1177/1933719114542029</doi><tpages>6</tpages></addata></record> |
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| ispartof | Reproductive sciences (Thousand Oaks, Calif.), 2015-02, Vol.22 (2), p.258-263 |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Ascitic Fluid - immunology Ascitic Fluid - metabolism Cell Proliferation - drug effects Colchicine - pharmacology Cytoprotection Disease Models, Animal Down-Regulation Embryology Endometriosis - immunology Endometriosis - metabolism Endometriosis - pathology Endometriosis - prevention & control Endometrium - drug effects Endometrium - immunology Endometrium - metabolism Endometrium - pathology Endometrium - transplantation Female Medicine & Public Health Obstetrics/Perinatology/Midwifery Original Article Rats, Wistar Reproductive Medicine Time Factors Tumor Necrosis Factor-alpha - blood Tumor Necrosis Factor-alpha - metabolism |
| title | Protective Effects of Colchicine in an Experimental Rat Endometriosis Model: Histopathological Evaluation and Assessment of TNF-α Levels |
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