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机构地区:[1]辽宁医学院附属第一医院妇产科,锦州121001 [2]辽宁医学院
出 处:《北京医学》2010年第11期883-886,共4页Beijing Medical Journal
摘 要:目的探讨人参皂甙Rg3(ginsenoside Rg3,GS-Rg3)诱导人子宫内膜癌Ishikawa细胞株凋亡的作用及其信号通路。方法 Ishikawa细胞分为实验组和对照组。采用MTT法观察GS-Rg3对Ishikawa细胞生长的抑制作用,Transwell小室分析细胞体外的侵袭力,流式细胞术观察GS-Rg3对Ishikawa细胞周期的影响,Western blotting检测Caspase-3、P65蛋白的表达。结果经GS-Rg3作用后,Ishikawa细胞的生长受到明显的抑制(P<0.05),细胞侵袭力降低,S期细胞数增加,G2/M期细胞数减少(P<0.05),凋亡细胞数增加。Western blot检测显示,GS-Rg3作用Ishikawa细胞48h后,随着GS-Rg3浓度的增加,Caspase-3蛋白表达增加,P65蛋白表达下调,各实验组与对照组间比较有显著性差异(P<0.05)。结论 GS-Rg3可以通过下调P65蛋白的表达阻断NF-кB信号途径,抑制人子宫内膜癌Ishikawa细胞增殖,促进其凋亡。Objective To study the effect of Ginsenoside Rg3 (GS -Rg3) inhibits growth of human endometrial cancer cell lines Ishikawa by inhibiting NF-кB pathway. Methods Ishikawa cells were divided into Rg3 treatment group and blank control group. The apoptosis effect of GS -Rg3 on Ishikawa cells was examined using MTT assays. Flow cytometric analysis of cell cycle and apoptosis was used to determine the effect of GS-Rg3 on the Ishikawa cells and to assess potential toxic side effects of GS-Rg3. Ability of invasion was compared with transwell chambermode. The protein expressions of caspase-3 and P65 in Ishikawa cells were detected by western blot. Results Treatment with GS -Rg3 resulted in preferential cell death in Ishikawa cells (P 0.05), the invasion of Ishikawa cell was also decreased. Ishikawa cells were increased in cell cycle S phase, the G2/M phase cells were reduced (P 0.05), while the number of apoptotic cells was increased. The cellular caspase-3 level was elevated whereas the P65 level was decreased in GS-Rg3-treated Ishikawa cells after 48 h in comparison to those in the control cells.There was significant difference in the experimental group when compared with the blank control group in the protein expression levels (P 0.05). Conclusion GS-Rg3 can inhibit Ishikawa cell proliferation and promote cell apoptosis by down-regulating the NF-кB signaling pathway.
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