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Resveratrol suppresses inflammatory responses in endometrial stromal cells derived from endometriosis: A possible role of the sirtuin 1 pathway
Author(s) -
Taguchi Ayumi,
WadaHiraike Osamu,
Kawana Kei,
Koga Kaori,
Yamashita Aki,
Shirane Akira,
Urata Yoko,
Kozuma Shiro,
Osuga Yutaka,
Fujii Tomoyuki
Publication year - 2014
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.12252
Subject(s) - resveratrol , sirtuin 1 , endometriosis , stromal cell , medicine , inflammation , sirtuin , tumor necrosis factor alpha , cancer research , activator (genetics) , immunology , pharmacology , biology , downregulation and upregulation , acetylation , receptor , gene , biochemistry
Abstract Aim Endometriosis is a chronic inflammatory disease. Sirtuin 1 ( SIRT1 ) plays a role in regulation of inflammation. The role of SIRT1 in endometriosis remains unknown. We here addressed the anti‐inflammatory effects of SIRT1 on endometriosis. Methods The expression of SIRT1 in human ovarian endometriomas and eutopic endometria were examined using immunohistochemistry and reverse transcription polymerase chain reaction ( RT–PCR ). Endometriotic stromal cells ( ESC ) obtained from endometriomas were exposed to either resveratrol or sirtinol, an activator or inhibitor of sirtuins, respectively, and tumor necrosis factor ( TNF )‐α‐induced interleukin ( IL )‐8 release from the ESC was assessed at m RNA and protein levels. Results Both immunochemistry and RT–PCR demonstrated that SIRT1 was expressed in ESC and normal endometrial stromal cells. Resveratrol suppressed TNF ‐α‐induced IL ‐8 release from the ESC in a dose‐dependent manner while sirtinol increased IL ‐8 release. Conclusion These opposing effects of SIRT1 ‐related agents suggest that IL ‐8 release from the ESC is modulated through the SIRT1 pathway. Resveratrol may have the potential to ameliorate local inflammation in endometriomas.

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