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Reproductive Biomedicine
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Volume 11, Issue 5 (7-2013)
IJRM 2013, 11(5): 415-0 |
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Zhang Y, Cao H, Yu Z, Peng H, Zhang C. Curcumin inhibits endometriosis endometrial cells by reducing estradiol production. IJRM 2013; 11 (5) :415-0
URL: http://ijrm.ir/article-1-417-en.html
URL: http://ijrm.ir/article-1-417-en.html
1- Reproductive Medicine Center, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China
2- Department of Orthopedic Surgery, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China
3- Reproductive Medicine Center, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China , 33556511@qq.com
2- Department of Orthopedic Surgery, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China
3- Reproductive Medicine Center, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China , 33556511@qq.com
Abstract: (3234 Views)
Background: Endometriosis is a complex estrogen-dependent disease that is defined as the presence of endometrial gland and stroma outside the uterine cavity. Although the exact mechanism for the development of endometriosis remains unclear, there is a large body of research data and circumstantial evidence that suggests a crucial role of estrogen in the establishment and maintenance of this disease.
Objective: This study is an attempt to assess the effect of curcumin on inhibiting endometriosis endometrial cells and to investigate whether such an effect is mediated by reducing estradiol production.
Materials and Methods: Endometriotic stromal cells, normal endometrial stromal cells, endometriotic epithelial cells and normal endometrial epithelial cells were isolated and cultured. E2 value of cells and the effect of curcumin on cell proliferation were evaluated. Finally, effect of curcumin on E2 assay was detected.
Results: Electrochemiluminescence immunoassay results showed that E2 value of endometriotic epithelial cells was higher than the endometriotic stromal cells (p=0.037), while the expression of E2 in normal endometrial stromal and epithelial cells was extremely low. WST-8 result showed, compared with endometrial stromal cells, ectopic endometriotic stromal cells had a higher growth rate. After intervene with curcumin (10μmol/L, 30μmol/L and 50μmol/L) for 0-96h, the number of endometriotic stromal cells was reduced and cells growth slowed, compared with 0μmol/L group. Compared with 0μmol/L group, E2 level was lower after treatment with curcumin, especially in 30μmol/L and 50μmol/L group.
Conclusion: In summary, in this study we found that E2 is important in ectopic endometrium, and epithelial cell is in dominant position with E2 secretion. Curcumin was able to suppress the proliferation of endometrial cells by reducing the E2 value
Objective: This study is an attempt to assess the effect of curcumin on inhibiting endometriosis endometrial cells and to investigate whether such an effect is mediated by reducing estradiol production.
Materials and Methods: Endometriotic stromal cells, normal endometrial stromal cells, endometriotic epithelial cells and normal endometrial epithelial cells were isolated and cultured. E2 value of cells and the effect of curcumin on cell proliferation were evaluated. Finally, effect of curcumin on E2 assay was detected.
Results: Electrochemiluminescence immunoassay results showed that E2 value of endometriotic epithelial cells was higher than the endometriotic stromal cells (p=0.037), while the expression of E2 in normal endometrial stromal and epithelial cells was extremely low. WST-8 result showed, compared with endometrial stromal cells, ectopic endometriotic stromal cells had a higher growth rate. After intervene with curcumin (10μmol/L, 30μmol/L and 50μmol/L) for 0-96h, the number of endometriotic stromal cells was reduced and cells growth slowed, compared with 0μmol/L group. Compared with 0μmol/L group, E2 level was lower after treatment with curcumin, especially in 30μmol/L and 50μmol/L group.
Conclusion: In summary, in this study we found that E2 is important in ectopic endometrium, and epithelial cell is in dominant position with E2 secretion. Curcumin was able to suppress the proliferation of endometrial cells by reducing the E2 value
Type of Study: Original Article |
References
1. Garcia Manero M, Olartecoechea B, Royo Manero P, Auba M, Lopez G. Endometriosis. Rev Med Univ Navarra 2009; 53: 4-7.
2. Giretti MS, Fu XD, De Rosa G, Sarotto I, Baldacci C, Garibaldi S, et al. Extra-nuclear signalling of estrogen receptor to breast cancer cytoskeletal remodelling, migration and invasion. PLoS One 2008; 3: e2238. [DOI:10.1371/journal.pone.0002238]
3. Ito K, Utsunomiya H, Yaegashi N, Sasano H. Biological roles of estrogen and progesterone in human endometrial carcinoma-new developments in potential endocrine therapy for endometrial cancer. Endocr J 2007; 54: 667-679. [DOI:10.1507/endocrj.KR-114]
4. Dassen H, Punyadeera C, Kamps R, Delvoux B, Van Langendonckt A, Donnez J, et al. Estrogen metabolizing enzymes in endometrium and endometriosis. Hum Reprod 2007; 22: 3148-3158. [DOI:10.1093/humrep/dem310]
5. Basnet P, Skalko-Basnet N. Curcumin: an anti-inflammatory molecule from a curry spice on the path to cancer treatment. Molecules 2011; 16: 4567-4598. [DOI:10.3390/molecules16064567]
6. Taylor RA, Leonard MC. Curcumin for inflammatory bowel disease: a review of human studies. Altern Med Rev 2011; 16: 152-156.
7. Darvesh AS, Aggarwal BB, Bishayee A. Curcumin and liver cancer: a review. Curr Pharm Biotechnol 2012; 13: 218-228. [DOI:10.2174/138920112798868791]
8. Rizner TL. Estrogen metabolism and action in endometriosis. Mol Cell Endocrinol 2009; 307: 8-18. [DOI:10.1016/j.mce.2009.03.022]
9. Nothnick WB. Endometriosis: in search of optimal treatment. Minerva Ginecol 2010; 62: 17-31.
10. Zhang Y, Cao H, Hu YY, Wang H, Zhang CJ. Inhibitory effect of curcumin on angiogenesis in ectopic endometrium of rats with experimental endometriosis. Int J Mol Med 2011; 27: 87-94.
11. Taylor HS, Osteen KG, Bruner-Tran KL, Lockwood CJ, Krikun G, Sokalska A, et al. Novel therapies targeting endometriosis. Reprod Sci 2011; 18: 814-823. [DOI:10.1177/1933719111410713]
12. Vouk K, Smuc T, Guggenberger C, Ribic-Pucelj M, Sinkovec J, Husen B, Tet al. Novel estrogen-related genes and potential biomarkers of ovarian endometriosis identified by differential expression analysis. J Steroid Biochem Mol Biol 2011; 125: 231-242. [DOI:10.1016/j.jsbmb.2011.03.010]
13. Takahashi K, Nagata H, Kitao M. Clinical usefulness of determination of estradiol level in the menstrual blood for patients with endometriosis. Nihon Sanka Fujinka Gakkai Zasshi 1989; 41: 1849-1850.
14. Alborzi S, Hamedi B, Omidvar A, Dehbashi S, Alborzi M. A comparison of the effect of short-term aromatase inhibitor (letrozole) and GnRH agonist (triptorelin) versus case control on pregnancy rate and symptom and sign recurrence after laparoscopic treatment of endometriosis. Arch Gynecol Obstet 2011; 284: 105-110. [DOI:10.1007/s00404-010-1599-6]
15. Bohrer J, Chen CC, Falcone T. Persistent bilateral ureteral obstruction secondary to endometriosis despite treatment with an aromatase inhibitor. Fertil Steril 2008; 90: e7-9. [DOI:10.1016/j.fertnstert.2008.03.040]
16. Fatemi HM, Al-Turki HA, Papanikolaou EG, Kosmas L, De Sutter P, Devroey P. Successful treatment of an aggressive recurrent post-menopausal endometriosis with an aromatase inhibitor. Reprod Biomed Online 2005; 11: 455-457. [DOI:10.1016/S1472-6483(10)61140-6]
17. Yang S, Fang Z, Gurates B, Tamura M, Miller J, Ferrer K, et al. Stromal PRs mediate induction of 17beta-hydroxysteroid dehydrogenase type 2 expression in human endometrial epithelium: a paracrine mechanism for inactivation of E2. Mol Endocrinol 2001; 15: 2093-2105.
18. Lessey BA, Gui Y, Apparao KB, Young SL, Mulholland J. Regulated expression of heparin-binding EGF-like growth factor (HB-EGF) in the human endometrium: a potential paracrine role during implantation. Mol Reprod Devl 2002; 62: 446-455. [DOI:10.1002/mrd.10129]
19. Beliard A, Noel A, Goffin F, Frankenne F, Foidart JM. Role of endocrine status and cell type in adhesion of human endometrial cells to the peritoneum in nude mice. Fertil Steril 2002; 78:973-978. [DOI:10.1016/S0015-0282(02)03370-8]
20. Sankar P, Telang AG, Manimaran A. Curcumin protects against cypermethrin-induced genotoxicity in rats. Environ Toxicol Pharmacol 2010; 30: 289-291. [DOI:10.1016/j.etap.2010.07.005]
21. Huang AC, Chang CL, Yu CS, Chen PY, Yang JS, Ji BC, et al. Induction of apoptosis by curcumin in murine myelomonocytic leukemia WEHI-3 cells is mediated via endoplasmic reticulum stress and mitochondria-dependent pathways. Environ Toxicol 2013; 28: 255-266. [DOI:10.1002/tox.20716]
22. Mito S, Thandavarayan RA, Ma M, Lakshmanan A, Suzuki K, Kodama M, et al. Inhibition of cardiac oxidative and endoplasmic reticulum stress-mediated apoptosis by curcumin treatment contributes to protection against acute myocarditis. Free Radic Res 2011; 45: 1223-1231. [DOI:10.3109/10715762.2011.607252]
23. Bachmeier BE, Mirisola V, Romeo F, Generoso L, Esposito A, Dell'eva R, et al. Reference profile correlation reveals estrogen-like trancriptional activity of Curcumin. Cell Physiol Biochem 2010; 26: 471-482. [DOI:10.1159/000320570]
24. Singh M, Singh N. Curcumin counteracts the proliferative effect of estradiol and induces apoptosis in cervical cancer cells. Mol Cell Biochem 2011; 347: 1-11. [DOI:10.1007/s11010-010-0606-3]
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