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作 者:黎雅静 洪雪 LI Yajing;HONG Xue(Nanfang Hospital of Nanfang Medical University,Guangzhou 510515,China)
机构地区:[1]南方医科大学南方医院,广州510515 [2]广东省肾脏病研究所
出 处:《山东医药》2018年第34期29-32,共4页Shandong Medical Journal
基 金:广西药用资源化学与药物分子工程重点实验室;教育部重点实验室开放课题(CMEMR2015-B10)
摘 要:目的观察芦荟大黄素(AE)对人肝癌Hep G2细胞端粒酶活性的影响,并探讨其可能的分子机制。方法取对数生长期的Hep G2细胞,分别以终浓度为0、10、30、50μmol/L的AE作用24 h;收集Hep G2细胞,采用端粒重复序列扩增技术(TRAP)测定Hep G2细胞端粒酶活性,分别以Western blotting、PCR法检测Hep G2细胞中的h TERT、c-myc蛋白和基因表达水平。结果以终浓度为0、10、30、50μmol/L的AE作用Hep G2细胞24 h,其端粒酶活性分别为0.707±0.001、0.546±0.008、0.338±0.001、0.214±0.009;随着AE浓度升高,Hep G2细胞的端粒酶活性下降,且30、50μmol/L与0μmol/L AE作用的Hep G2细胞端粒酶活性差异有统计学意义(P均<0.05)。随着AE浓度升高,Hep G2细胞h TERT、c-myc mRNA和蛋白表达水平均下降;其中,h TERT、c-myc mRNA和蛋白在50μmol/L,h TERT mRNA在30μmol/L,与0μmol/L差异有统计学意义(P均<0.05)。结论 AE可通过下调cmyc和h TERT表达从而抑制Hep G2细胞端粒酶活性。Objective To investigate the effect of aloe-emodin (AE) on telomerase activity of human liver cancer HepG2 cells as well as its possible mechanisms.Methods HepG2 cells in the logarithmic phase were divided into 4 groups which were treated with 0, 10, 30, and 50 μmol/L AE for 24 h. Telomeric repeat amplification protocol (TRAP) assay was performed to assess the telomerase activity in each group. The mRNA and protein levels of c-myc and human telomerase reverse transcriptase (hTERT) were investigated by PCR and Western blotting. Results After 24-hour treatment of 0, 10, 30, and 50 μmol/L AE, the telomerase activity in HepG2 cells was 0.707±0.001, 0.546±0.008, 0.338 ± 0.001 , and 0.214±0.009, respectively; the telomerase activity decreased as the AE concentration increased, and the telomerase activity in the 30 and 50 μmol/L AE groups was significantly lower than that in the 0 μmol/L group ( P 〈0.05). The mRNA and protein levels of hTERT and c-myc decreased as the AE concentration increased, and the mRNA and protein levels of hTERT and c-myc of the 50 μmol/L group, the mRNA level of hTERT of the 30 μmol/L group was significantly lower than that of the 0 μmol/L group (all P 〈0.05).Conclusion AE can inhibit the telomerase activity in HepG2 cells through down-regulating the c-myc and hTERT expression.
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