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作 者:李覃[1] 王伟[2] 张实[3] 邢杰[1] 王增田[4]
机构地区:[1]天津武警后勤学院病原生物与免疫学教研室,天津300309 [2]天津武警后勤学院附属医院,天津300162 [3]天津武警后勤学院实验动物中心,天津300162 [4]天津武警后勤学院临床医学系,天津300309
出 处:《中国药理学通报》2014年第2期186-191,共6页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 81202843);天津市应用基础与前沿技术研究计划(No 11JCYBJC14600);中国博士后科学基金特别资助(No 201104796);中国博士后科学基金面上项目(No 20090461498)
摘 要:目的初步探讨白藜芦醇(Resveratrol,Res)的抗肝癌作用及其分子机制。方法建立移植性肝癌小鼠模型,口服给予Res进行干预,分析肿瘤生长状况。然后采用Real-time PCR、RT-PCR等方法检测转录因子Foxp3及微小核糖核酸-21(miR-21)的基因表达,Western blot分析信号转导子与转录激活子3(STAT3)的活性表达,流式细胞术观察CD4+CD25+T细胞数量的变化。结果与荷瘤对照组相比,Res给药组CD4+CD25+T细胞数量和Foxp3表达均明显降低,同时miR-21表达减少,该效应或许与其下调STAT3磷酸化活性水平密切相关。结论 Res可能通过调控STAT3信号分子及miR-21表达,抑制调节性T细胞产生,改变肿瘤微环境,从而发挥抗肝癌作用。Aim To investigate the effect of resveratrol (Res) on hepatocellular carcinoma and its molecular mechanism. Methods The mouse models of hepato- cellular carcinoma were induced by injecting H22 cells, which were administered orally with Res. Then, real-time PCR and RT-PCR were used to detect the ex-pression of transcription factor Foxp3 and microRNA-21 (miR-21) mRNA. Western blot assay was applied to measure the signal transducers and activators of tran- scription 3 (STAT3) activation. Besides, the percent-age of CD4 + CD25 + T cells was detected by flow cy-tometry. Results The production of CD4 + CD25 + Tcells decreased remarkably in Res-treated mice com- pared with the tumor control group, accompanied with the low expression of Foxp3 mRNA. Furthermore, Res could also inhibit the expression of miR-21, which might be responsible for the down-regulation of phos-phorylated-STA33 level. Conclusion Res might con- tribute to the anti-hepatocellular carcinoma action by regulating STAT3 and miR-21, which would be helpful to improve the tumor microenvironment through inhibi-ting CD4 + CD25 + T cells.
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