The Journal of Korean Obstetrics and Gynecology (대한한방부인과학회지)
- Volume 20 Issue 2
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- Pages.25-42
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- 2007
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- 1229-4292(pISSN)
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- 2508-3619(eISSN)
Induced apoptosis in human Uterine Leiomyoma Cells by treatment with Chiljehyangbu-hwan
칠제향부환(七製香附丸)이 자궁근종세포의 성장억제와 세포자멸사에 미치는 영향
- Kim, Seuk-Jung (Dept. of OB & GY, Oriental Medicine, Daeguhaany University) ;
- Beak, Seung-Hee (Odri women's Traditional Korean Medical Clinic) ;
- Kim, En-Ha (Dept. of Original text and Medical history, Oriental Medicine, Daeguhaany University) ;
- Kim, Dong-Chul (Dept. of OB & GY, Oriental Medicine, Daeguhaany University)
- 김석중 (대구한의대학교 한의과대학 부인과교실) ;
- 백승희 (오드리 여성한의원) ;
- 김은하 (대구한의대학교 한의과대학 원전의사학교실) ;
- 김동철 (대구한의대학교 한의과대학 부인과교실)
- Published : 2007.05.29
Abstract
Purpose : Uterine leiomyoma (fibroids) are benign smooth muscle tumors originating from the myometrium. These benign neoplasms of monoclonal origin are typically diagnosed during the reproductive years, occurring only after puberty and tending to regress after menopause. In the present study we used Chiljehyangbu-hwan to determine its growth inhibitory effect and apoptosis in human uterine leiomyoma cells. Methods : Primary cultured human uterine leiomyoma cells were treated with Chiljehyangbu-hwan. Cell viability analysis was analyzed by MTS assay and FACS was performed to ascertain the effects Chiljehyangbu-hwan. DNA fragmentation analysis and casapase-3 activity test were done. Expression of apoptosis related proteins were evaluated by Western blot analysis. Results : Cell viability was significantly influenced by Chiljehyangbu-hwan treatment in a dose-dependent manner in leiomyoma cells compare to normal myometrial cells. FACS showed that Chiljehyangbu-hwan induced Sub G1 arrest. DNA fragmentation assay was carried out and apoptosis was detected. Activation of caspase-3, down-regulation of Bcl-2, with concomitant increased expression in Bid and Bax were observed. Chiljehyangbu-hwan treatment of uterine leiomyoma cells resulted in a concentration-dependent cell death induced via the mitochondrial pathway.