摘要
目的:探讨金雀异黄素对白细胞介素1α(IL-1α)刺激破骨样细胞组织蛋白酶K(CK)表达的作用。方法:从人骨巨细胞瘤组织中纯化出破骨样细胞(OCLs),用不同浓度的金雀异黄素或17β-雌二醇(17β-E2)孵育,并设空白对照组和阳性对照组,采用RT-PCR和Western blot方法,观察IL-1α刺激后CK的表达。结果:与空白对照组相比,IL-1α刺激CK表达显著增加(P<0.01);金雀异黄素在转录水平下调IL-1α刺激后CK的表达,且呈剂量依赖关系(r=0.68,P<0.01);金雀异黄素下调IL-1α刺激后CK的蛋白表达,且呈剂量依赖关系(r=0.61,P<0.01)。雌激素受体拮抗剂ICI 182.780可以部分抑制金雀异黄素的上述作用。结论:金雀异黄素可通过破骨样细胞的雌激素受体部分抑制IL-1α刺激后CK的表达。
AIM: To discuss the effects of phytoestrogenic-genistein on cathepsin K (CK) expression stimulated by interleukin-1α (IL-1α) in osteoclast-like cells (OCLs) . METHODS: The OCLs were isolated from tissue of human giant cell tumor of bone (GCT). The cells treated with reagents were divided into 7 groups including control (treated with phenol red-free-DMEM), vehicle (treated with 1.2 nmol·L^-1 IL-1α), 10^-10 - 10^-6 genistein, genistein+ ICI 182.780, and 17β-estrodiol (17β-E2) group. The cells were treated with 1.2 nmol·L^-1 IL-1α after pre-treated with genistein or 17β-E2 for 48 h (excluded the control group) . Expression of CK was determined by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot in OCLs stimulated by IL-1α in the presence of genistein or 17β-E2. RESULTS: The obvious increase of expression of CK by IL-1α in vehicle group was noted in comparing with control group (P 〈 0.01) . Genistein down-regulated CK gene expression stimulated by IL-1α at the transcription level in a dose-dependent manner (r = 0.68, P 〈 0.01) . Genistein down-regulated CK protein expression stimulated by IL-1α also in a dose-dependent manner (r = 0.61, P 〈 0.01 ). The effects of genistein were abrogated partly after treatment with the estrogen receptor antagonist ICI 182.780. CONCLUSION: Genistein inhibits CK expression stimulated by IL-1α partly through estrogen receptor in OCLs.
出处
《中国新药与临床杂志》
CAS
CSCD
北大核心
2006年第10期725-729,共5页
Chinese Journal of New Drugs and Clinical Remedies
基金
This work is supported by the Natural Science Foundation (No.Hubei Province 2004ABA251) and the Science Foundation of Huazhong University of Science and Technology (No.200301)