目的检测内质网应激ATF6-CHOP通路的激活水平,以探究单宁酸(TA)联合顺铂(CDDP)抗肝癌的分子机制。方法用180μmol/L TA、0.9μg/m L CDDP单独用药或者联合用药处理肝癌Hep G2细胞24和48 h后,利用实时荧光定量PCR(q-RT-PCR)、蛋白免疫印迹(Western Blot)技术检测细胞ATF6(ATF6α)、ATF6B(ATF6β)和CHOP的表达水平。结果药物处理24和48 h后,与对照组相比,TA组、CD-DP组和联合用药组ATF6 m RNA和蛋白水平、ATF6B蛋白水平、CHOP m RNA和蛋白水平均显著升高(P<0.01或P<0.05)。结论 TA能够联合CDDP增强肝癌Hep G2细胞内质网应激ATF6-CHOP通路的激活水平,ATF6-CHOP通路可能是TA和CDDP协同抗肝癌的分子机制之一。
【英文摘要】
Objective To detect the activation levels of endoplasmic reticulum stress ATF6-CHOP path-way,and to investigate the molecular mechanism of tannic acid(TA)combined with cisplatin(CDDP)against he-patocellular carcinoma. Methods Hep G2 cells were cultured with 180 μM TA or/and 0.9 μg/ml CDDP for 24 h or48 h. The levels of ATF6(ATF6α),ATF6B(ATF6β)and CHOP were analyzed by real-time fluorescence quanti-tative PCR(q-RT-PCR)and western blot. Results We found that after 24 h or 48 h,compared with the controlgroup,A...
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