摘要
目的:探讨姜黄素对人甲状腺癌B-CPAP细胞生长、凋亡的影响及可能的作用机制。方法:采用含有不同浓度(10μmol/L、20μmol/L、40μmol/L)姜黄素的培养基培养人甲状腺癌B-CPAP细胞12 h、24 h、36h、48 h、72 h、96 h,应用MTT实验观察姜黄素对B-CPAP细胞生长的影响;采用含有不同浓度姜黄素的培养基培养人甲状腺癌B-CPAP细胞36 h、48 h、72 h、96 h,应用Annexin V/PI染色评价姜黄素诱导B-CPAP细胞凋亡的作用;应用蛋白印迹法检测姜黄素对ERK通路、Bax、Bcl-2表达的影响。结果:浓度为10μmol/L、20μmol/L、40μmol/L的姜黄素培养甲状腺癌B-CPAP细胞,随着培养时间延长,各浓度下细胞生长抑制率、细胞凋亡率均逐渐增高(P <0. 05);且随着浓度增加,相同时间点的细胞生长抑制率、细胞凋亡率亦逐渐增高(P <0. 05)。与空白组比较,姜黄素培养72 h后,B-CPAP细胞的H-Ras、p-Raf-B、p-ERK1/2、Bcl-2蛋白表达水平明显降低(P <0. 05),Bax蛋白表达水平水平明显升高(P <0. 05)。结论:姜黄素能够抑制人甲状腺癌B-CPAP细胞生长,诱导细胞凋亡,其机制可能与抑制H-Ras蛋白、ERK信号通路蛋白表达及上调Bax表达、下调Bcl-2表达有关。
Objective: To investigate the effect of curcumin on the growth and apoptosis of human thyroid carcinoma B-CPAP cells and its possible mechanism. Methods: The human thyroid carcinoma B-CPAP cells were cultured in medium containing different concentrations( 10 μmol/L,20 μmol/L,40 μmol/L) of curcumin for 12 h,24 h,36 h,48 h,72 h and 96 h. The effect of curcumin on the growth of B-CPAP cells was observed by MTT. The human thyroid carcinoma B-CPAP cells were cultured in medium containing different concentrations of curcumin for 36 h,48 h,72 h and 96 h. The effects of curcumin in inducing apoptosis of B-CPAP cells were evaluated with Annexin V/PI staining,and the effect of curcumin on ERK pathway,Bax and Bcl-2 expression was detected by Western blot.Results: The growth inhibition rate and apoptosis rate of human thyroid carcinoma B-CPAP cells cultured in medium containing 10 μmol/L,20 μmol/L and 40 μmol/L of curcumin increased gradually with the prolongation of culture time( P < 0. 05). With the increase of concentration,the growth inhibition rate and the apoptosis rate also increased gradually at the same time point( P < 0. 05). After 72 h of culture,the expression levels of H-Ras,p-Raf-B,p-ERK1/2 and Bcl-2 proteins in B-CPAP cells were significantly lower,while the expression level of Bax protein was significantly higher than that in the blank control group( P < 0. 05). Conclusion: Curcumin can inhibit the growth and induce apoptosis of human thyroid carcinoma B-CPAP cells. The mechanism may be related to inhibiting the expression of H-Ras protein and ERK signaling pathway,up-regulating the expression of Bax and down regulating the expression of Bcl-2.
作者
孙巍
Sun Wei(Department of General Surgery,the Zhumadian Central Hospital, Henan Zhumadian 463000,China.)
出处
《现代肿瘤医学》
CAS
2019年第2期183-187,共5页
Journal of Modern Oncology
基金
河南省卫生和计划委员会基础研究项目(编号:JH201703054)
