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作 者:韦鹏涯[1] 浦洪琴[2] 韦星[3] 李朝敢[3] 农嵩[3]
机构地区:[1]右江民族医学院微生物学教研室,广西百色533000 [2]右江民族医学院解剖学教研室,广西百色533000 [3]右江民族医学院生物化学与分子生物学教研室,广西百色533000
出 处:《右江医学》2008年第4期381-383,共3页Chinese Youjiang Medical Journal
基 金:右江民族医学院2005年度科研立项资助项目(右医院字[2005]99号)
摘 要:目的观察中药抗癌灵(Kangailing,Ka)对人肝癌SMMC-7721细胞增殖的影响并探讨其可能分子机制。方法提取、配制不同抗癌灵生药浓度,作用于体外培养的人肝癌SMMC-7721细胞,采用MTT法检测细胞增殖抑制率,流式细胞仪法检测凋亡率,二步法免疫组化检测野生型P53、NF-кB P65和Bcl-2蛋白表达变化。结果与正常对照组比较,Ka各浓度组细胞抑制率显著上升(P<0.001),细胞凋亡率明显升高(P<0.01或P<0.001),P53蛋白表达显著上升(P<0.001),NF-кB和Bcl-2蛋白表达明显下降(P<0.001)。结论Ka通过诱导细胞凋亡而抑制肝癌SMMC-7721细胞增殖,其分子机制可能与上调野生型P53蛋白表达,下调NF-кB P65和Bcl-2蛋白表达有关。Objective To observe the effects of traditional Chinese medicine Kangailing on proliferation in hu- man hepatoma SMMC-7721 cell lines in vitro and investigate its possible molecular mechanism. Methods The proliferation inhibitory rate was evaluated by MTT assay. Apoptotic rate was determined by flow cytometry. The expression of wild type P53,NF-κB P65and Bcl-2 proteins were detected by two-step immunhistochemical staining. Results The cell inhibitory rate and apoptotic rate and the expression of P53 Protein of Ka treatment groups increased obviously than that of control group ( P 〈0. 001), while NF-κB P65and Bcl-2 Proteins were decreased markedly( P 〈0. 001). Conclusion Kangailing could inhibit the proliferation of SMMC-7721 cells in vitro by inducing cancer cell apoptosis, and its molecular mechanism may be associated with the up-regulation ofthe expression of wild type P53 protein and down-regulation of the expression of NF-κB P65 and Bcl-2 proteins.
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