[Effects of ginsenoside Rh2(GS-Rh2) on cell cycle of Eca-109 esophageal carcinoma cell line].
Zhongguo Zhong Yao Za Zhi
; 30(20): 1617-21, 2005 Oct.
Article
en Zh
| MEDLINE
| ID: mdl-16422547
OBJECTIVE: To investigate the effects of ginsenoside Rh2 (GS-Rh2) on growth inhibition and cell cycle of Eca-109 esophageal carcinoma cell line in culture. METHOD: The effects of GS-Rh2 on cell growth inhibition was detected by MTT assay. Cell cycle was analyzed by flow cytometry (FCM). Cell morphology was observed by a light microscope after HE staining. The protein expression of cell cycle components (cyclinE, CDK2, p21WAF1) were examined by immunocytochemistry and Western blot. The mRNA expression were examined by semiquantitative RT-PCR. RESULT: GS-Rh2 inhibited the proliferation of Eca-109 cells in dose and time-dependent manners. The inhibition rate was about 50% after 1-day treatment with 20 microg x mL(-1) GS-Rh2 x 20 microg x mL(-1) GS-Rh2 induced the mature differentiation and morphological reversion. With increasing dose of GS-Rh2 treatment, the cell number of G0/G1 phase was increased, whereas it decreased at S and G2/M phase. There was significant difference between 10, 20 microg x mL(-1) GS-Rh2 groups and the corresponding group without GS-Rh2 treatement. After treating cells by 20 microg x mL(-1) GS-Rh2 for 1, 2, 3 days individually, the protein and mRNA expression of both cyclinE and CDK2 reduced, while the expression of p21WAF1 enhanced gradually. CONCLUSION: GS-Rh2 could arrest Eca-109 cells at G0/G1 phase and induce cell differentiation tending to normal. Furthermore, GS-Rh2 had an effect on expression of cell cycle components (cyclinE, CDK2 and p21WAF1) to inhibit Eca-109 cell proliferation.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias Esofágicas
/
Medicamentos Herbarios Chinos
/
Ciclo Celular
/
Ginsenósidos
/
Panax
Límite:
Humans
Idioma:
Zh
Revista:
Zhongguo Zhong Yao Za Zhi
Asunto de la revista:
FARMACOLOGIA
/
TERAPIAS COMPLEMENTARES
Año:
2005
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
China