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Increased expression of glutathione by estradiol, tumor necrosis factor-alpha, and interleukin 1-beta in endometrial stromal cells

Title
Increased expression of glutathione by estradiol, tumor necrosis factor-alpha, and interleukin 1-beta in endometrial stromal cells
Authors
Lee S.R.Kim S.H.Lee H.W.Kim Y.-H.Chae H.D.Kim C.-H.Kang B.M.
Ewha Authors
이사라
SCOPUS Author ID
이사라scopus
Issue Date
2009
Journal Title
American Journal of Reproductive Immunology
ISSN
1046-7408JCR Link
Citation
vol. 62, no. 6, pp. 352 - 356
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Problem: The intracellular antioxidant system, based on glutathione (GSH), plays a key role in endometrial detoxification reactions and has been proposed to be involved in the pathogenesis endometriosis. This study was designed to evaluate whether estradiol (E2) and proinflammatory cytokines have any effects on expression of glutathione in endometrial stromal cells (ESCs). Method of study: Glutathione levels were measured utilizing high-performance liquid chromatography following in vitro culture and treatment of ESCs with estradiol, tumor necrosis factor-alpha (TNF-α) and interleukin 1-beta (IL-1β). Results: The GSH level in E2 (10-8 m) treatment group was significantly higher than in the control group at 48 h (P < 0.05). In vitro treatment of ESCs with TNF-α 10 ng/mL as well as E2 (10-8 m) plus TNF-α 10 ng/mL for 48 hr also led to a significant increase in GSH level (P < 0.05; P < 0.05, respectively). Both IL-1β 10 ng/mL and E2 (10-8 m) plus IL-1β 10 ng/mL for 48 hr increased GSH level significantly (P < 0.05; P < 0.05, respectively) as well. Conclusions: These findings might suggest that increased production of estradiol and proinflammatory cytokines in the peritoneal cavity possibly leads to the establishment of endometriosis through increased level of GSH. © 2009 John Wiley & Sons A/S.
DOI
10.1111/j.1600-0897.2009.00760.x
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의학전문대학원 > 의학과 > Journal papers
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