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作 者:侯伟[1] 覃华[1] 刘爽[2] 王颖[1] 刘南植[1] 赵秋[1] 田德安[1]
机构地区:[1]华中科技大学同济医学院附属同济医院消化内科,湖北省武汉市430030 [2]湖北省疾病预防控制中心卫生监测检验防护所,湖北省武汉市430079
出 处:《世界华人消化杂志》2008年第21期2354-2358,共5页World Chinese Journal of Digestology
摘 要:目的:研究姜黄素对缺氧条件下人肝癌细胞HepG2中缺氧诱导因子-1α(HIF-1α)表达的影响,并探讨其可能机制.方法:0、1、2、5、10μmol/L的姜黄素处理缺氧条件下的HepG2细胞6h后,用Western blot免疫印迹法和RT-PCR检测HIF-1α的蛋白及mRNA的表达;0μmol/L,10μmol/L姜黄素,10μmol/L姜黄素+10μmol/LMG-132处理缺氧条件下的HepG2细胞6h后,用Western blot检测HIF-1α和VEGF的蛋白水平.结果:HepG2细胞经1、2、5、10μmol/L的姜黄素处理后,HIF-1α蛋白水平与对照组(0μmol/L姜黄素处理)比较明显降低(F=79.81,P<0.01),且降低程度随着姜黄素处理浓度的增加而变大,但各剂量组HIF-1α的mRNA水平与对照组比较无显著性差异;蛋白酶体抑制剂MG-132可以逆转姜黄素所致的HepG2细胞内HIF-1α和VEGF蛋白表达抑制(F=68.47,83.79,均P<0.01).结论:姜黄素通过蛋白酶体途径,在转录后水平抑制缺氧HepG2细胞的HIF-1α表达.AIM: To study the effect of curcumin on hypoxia-inducible factor-1 alpha (HIF-1α) expression in HepG2 hepatocellular carcinoma cells under hypoxic conditions as well as the possible mechanism. METHODS: HepG2 ceils were treated with different concentrations (0, 1, 2, 5, 10 μmol/L) of curcumin under hypoxic conditions for 6 h. The protein and mRNA levels of HIF-1α were detected by Western blot and reverse transcriptionpolymerase chain reation (RT-PCR) respectively. Then HepG2 cells were treated with 0, 10 μmol/L curcumin, or 10 μmol/L curcumin plus 10 μmol/L MG-132 under hypoxic conditions for 6 h. The protein levels of HIF-1α and vascular endothelial growth factor (VEGF) were detected by Western blot. RESULTS: After HepG2 cells were co-incubated with curcumin (1-10 μmol/L) for 6 h, the protein level of HIF-la decreased significantly as compared with that in the control cells (0 μmol/L curcumin treatment ), in a dose-dependent manner (F = 79.81, P 〈 0.01), but the mRNA level of HIF-1α was not affected by curcumin. In the presence of MG-132, a proteasome inhibitor, the HIF-la and VEGF protein levels decreased by curcunmin was restored to the level of control cells (F = 68.47, 83.79, both P 〈 0.01). CONCLUSION: Curcumin suppresses HIF-la expression at post-transcriptional level in HepG2 cells under hypoxia, probably via proteasomedependent pathway.
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