|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | 霉酚酸对人结肠癌SW620细胞凋亡的诱导作用及其机制显示文摘研究霉酚酸(mycophenolic acid,MPA)对人结肠癌细胞株SW620凋亡诱导作用及其机制.MPA处理SW620细胞后,MTT法测细胞增殖抑制活性,Hoechst 33258染色法检验细胞核形态变化.提取DNA并电泳检验DNA断裂情况,流式细胞仪检测凋亡和细胞周期的影响,并检验MPA处理后细胞中Caspase-3活性.Caspase-3抑制剂z-DEVD-FMK及MPA共同作用SW620细胞,检验DNA断裂的逆转情况.结果表明:MPA有效抑制SW620细胞的增殖,IC50为0.11mol/L.在浓度高于1.0mol/L时,经过MPA处理后的细胞核呈现明显的固缩现象,基因组DNA断裂为DNA ladder.流式细胞仪的测定结果说明MPA使细胞生长周期停滞于G1/S期,并能够浓度、时间依赖诱导SW620细胞出现典型的Sub-G1凋亡峰.进一步的细胞Caspase-3活性分析结果证明MPA能剂量依赖地诱导细胞中Caspase-3的活性,Caspase-3抑制剂z-DEVD-FMK能够部分地逆转MPA诱导的凋亡,说明Caspase-3在凋亡过程中起到了非常重要的作用.因此,MPA能够部分通过激活细胞中Caspase-3途径有效诱导结肠癌细胞SW620的凋亡,这可能是MPA抑制细胞增殖的一个重要分子机制. | 栗若兰 郑智慧 路新华 张雪霞 董爱华 段宝玲 赵宝华 | 2013 | 河北师范大学学报(自然科学版)2013,37,5: | 2 |
| 2 | Effect of mycophenolate mofetil plus adriamycin on HepG-2 cells显示文摘AIM:To investigate the influence of mycophenolate mofetil(MMF)plus adriamycin(ADM)on hepatocellular carcinoma(HCC)cells. METHODS:HCC cells were treated with 100μg/ml of MMF alone(MMF group),1μg/mL of adriamycin(ADM group)alone,or a combination of the drugs(MMF+ ADM group).We performed an 3-[4,5-dimethylthiazol2-yl]-2,5-diphenyl tetrazolium bromide(MTT)assay to measure the growth inhibition rate of HCC cells.Flow cytometry was used to determine the percentage of cells in different phases of the cell cycle and the number of apoptotic cells.Hoechst 33258 staining revealed the morphological changes associated with apoptosis in HCC cells. RESULTS:The results of MTT assays revealed that monotherapy with ADM or MMF showed inhibition of cell growth,while MMF+ADM therapy afforded an inhibition rate of more than 90%with cell distribution in G1 and G2/M phase greater than that in S phase. MMF+ADM treatment also downregulated Bcl-2 expression markedly.The growth of HCC cells was markedly inhibited and apoptosis was enhanced in all the 3 groups.Compared with other 2 groups,the MMF +ADM group showed more obvious apoptosis of cells. CONCLUSION:The MMF plus ADM combination exerts remarkable inhibitory effects on the growth of HCC cells. | Yan-Kui Chu,Yi Liu,Ji-Kai Yin,Nan Wang,Liang Cai,Jian-Guo Lu,Department of General Surgery,Tangdu Hospital, Fourth Military Medical University,Xi’an 710038,Shaanxi Province,China | 2010 | World Journal of Hepatology2010,2,8: | 1 |
| 3 | Inhibitory effect of mycophenolate mofetil on human hepatocellular carcinoma cell line HepG-2显示文摘Objective:To investigate the inhibitory effect of mycophenolate mofetil on human hepatocellular carcinoma cell line HepG-2. Methods: HepG-2 cells were cultured in the presence of the different concentrations of mycophenolate mofetil in vitro. MTT assay was used to analyze the inhibition of cell viability conferred by mycophenolate mofetil. Cell apoptosis was observed using Hoechst33258 staining, and the percentage of HepG-2 cells at different cell cycles was determined through flow cytometry. The ability of cell adhesion was evaluated by in vitro adhesion assay. Gene expressions of factors (ICAM-1 and VCAM-1) were detected by RT-PCR. Results: Mycophenolate mofetil significantly inhibited the growth of HepG-2 cells by inducing the apoptosis of cells and this drug also inhibited the adhesion of HepG-2 cells in a dose-dependent manner. Marked morphological changes characterized in cell apoptosis were demonstrated through Hoechst33258 staining. In addition, mycophenolate mofetil decreased the proportion of S phase cells and increased that of G0/G1 phase cells. [3H]-Thymidine uptake assay indicated that the application of mycophenolate mofetil at different concentrations significantly inhibited the cell proliferation. RT-PCR identified the expression levels of ICAM-1 and VCAM-1 genes in liver cancer cells after cultured for 72 h with different concentrations of drug. An inverse relationship was found between the expressions of ICAM-1 and VCAM-1 and drug concentrations. Conclusion: Mycophenolate mofetil has remarkable inhibitory effect on hepatocarcinoma HepG-2 cells. | Chu Yankui Lu Jianguo Yin Jikai Cai Liang Liu Yi | 2009 | Journal of Medical Colleges of PLA(China)2009,24,4: | 1 |
| 4 | CK19和TGF-α在大鼠肝纤维化部分肝切除后残肝中的表达显示文摘目的检测肝纤维化大鼠部分肝切除后不同时间点CK19及TGF-α的表达,了解其胆管再生情况。方法雄性SD大鼠,对照组和实验组各35只。实验组腹腔注射CCl4制备肝纤维化模型,两组均进行肝部分切除术。进行免疫组织化学、HE染色,图像分析和数据统计。结果验组和对照组术后随时间延长CK19表达均呈增强趋势;实验组术后各时间点CK19的表达均高于对照组同时间点。实验组和对照组术后随时间延长TGF-α表达均呈上升趋势,但实验组上升速度明显较对照组缓慢;实验组术后0d、1d、3d的TGF-α表达高于对照组。结论 (1)肝纤维化大鼠肝部分切除后CK19呈现高表达,提示肝纤维化部分切除可以促进肝卵圆细胞的增殖和分化。(2)TGF-α对肝纤维化大鼠肝部分切除后肝卵圆细胞增殖及胆管再生的促进作用不明显。 | 岳学强 施相空 李娜娜 臧卫东 刘恒兴 | 2011 | 中国临床解剖学杂志2011,29,2: | 1 |
| 5 | 雷帕霉素对肝移植术后胆管细胞再生的影响显示文摘目的探讨白介素6(IL-6)/信号转导及转录激活因子3(STAT3)通路是否参与肝移植术后胆管上皮细胞(BEC)再生过程,以及免疫抑制剂雷帕霉素是否通过影响STAT3活化从而抑制BEC增殖。方法将大鼠随机分为5组:正常肝移植组(OLT)-1h、OLT-12h组(供肝分别冷保存1、12h后行原位肝移植术)、抗sIL-6R组(OLT-12h组术前1h静脉注射可溶性抗IL-6受体抗体16.7μg/k,术后每日给予相同剂量直至观察结束)、RPM组(OLT-12h组术前3d腹腔注射雷帕霉素0.05mg/kg,术后每日给予相同剂量直至观察结束)、sham组(假手术组),样本检测时间点为术后1、3、7、14d。测定血清碱性磷酸酶(ALP)、谷氨酰转肽酶(GGT)含量以评价胆道功能,并进行肝脏组织学检查;采用酶联免疫吸附法检测肝组织IL-6含量;实时定量RT—PCR法检测BEC内IL-6mllNA表达;Western印迹法检测BEC内磷酸化STAT3(p-STAT3)、细胞周期蛋白(eyclin)D1的蛋白表达水平;电泳迁移率变动分析法(EMSA)检测BEC内STAT3的DNA结合活性;免疫组化法测定BEC增殖情况。结果与sham组相比,OLT.1h组术后1、3d,血清GGT、ALP轻度、短暂升高:其中GGF分别为(69±6)U/L、(34±4)U/L,ALP分别为(86±9)U/L、(45±3)U/L,BEC损伤轻微。肝组织及BEC内IL-6含量、P—STAT3及cyclinD1表达略增加:其中肝组织IL-6含量分别为(273±20)ng/g、(159±18)ng/g,在BEC内IL-6mRNA表达分别为0.40±0.04、0.234-0.04,BEC内P—STAT3表达分别为0.420±0.023、0.230±0.040,而eyclinD1表达分别为0.580±0.023、0.420±0.015;STAT3的DNA结合活性也相应短暂增加,与sham组之间的积分吸光度(A)比值为38±10、22±7;BEC再生不明显。相反,OLT一12h组术后1d,血清GGT、ALP即明显升高,分别为(108±9)U/L、(189±14)U/L,BEC损伤严重,至术后14d才恢复正常。肝组织及BEC内IL-6含量增加:其中肝组织IL-6含量分别为(659±28)ng/g、(446±23)ng/g,在BEC内IL-6mRNA表达分别为0.73±0.06、0.54±0.04。BEC内P—STAT3和cyclinDl蛋白表达上调,其中BEC内P—STAT3分别为0.72±0.04、0.58±0.06,eyclinDl蛋白表达分别为0.88±0.04、0.74±0.07,STAT3的DNA结合活性明显增加,sham组的A值分别为45±16、31±12;BEC再生活跃。OLT.12h组经抗sIL-6R和RPM处理后,p-STAT3和cyclinDl表达明显降低,STAT3的DNA结合活性及BEC再生受到明显抑制,术后14d仍可见细胞损伤的形态学表现,ALP、GGT明显高于sham组水平。不同的是sIL-6R还能显著降低OLT-12h组肝内IL-6的表达,而RPM对IL-6的表达并无明显影响。结论IL-6/STAT3信号通路介导肝移植术后BEC的再生/修复过程,雷帕霉素通过抑制STAT3活化从而影响BEC的再生,可能对肝移植术后胆道功能的恢复产生不利影响。 | 陈莉萍 郭毅斌 石炳毅 | 2011 | 中华医学杂志2011,91,22: | 1 |
| 6 | CK19和PCNA在肝纤维化大鼠部分肝切除后再生肝中的表达显示文摘目的检测肝纤维化大鼠部分肝切除后不同时点CK19及PCNA的表达,了解胆管再生情况。方法雄性SD大鼠,对照组和实验组各42只,实验组腹腔注射CCl4制备肝纤维化模型,两组均进行部分肝切除术,在不同时点取材后利用HE、免疫组化及免疫荧光双标染色等方法检测CK19和PCNA的表达情况。结果实验组和对照组术后随时间延长CK19表达均呈增强趋势,且实验组术后各时间点CK19的表达均高于对照组同时间点。两组PCNA的表达量都随时间推移逐步升高,但实验组大鼠明显上升缓慢,持续时间延长,表达高峰晚于对照组出现。结论 (1)肝纤维化大鼠部分肝切除能刺激肝卵圆细胞增殖和向胆管细胞的分化,而正常大鼠部分肝切除后再生肝中的胆管上皮细胞主要来源于原有细胞的代偿性增生。(2)术前肝纤维化大鼠的肝脏细胞就出现了增殖修复,术后由于肝纤维化大鼠本身肝脏受到伤害,因此肝脏的有效再生细胞数低于正常肝脏。 | 方方 刘前进 岳学强 李娜娜 刘恒兴 | 2012 | 中国临床解剖学杂志2012,30,5: | 1 |
| 7 | 霉酚酸酯对人肝癌细胞HepG-2抑制作用的研究显示文摘目的:研究霉酚酸酯体外对细胞生长抑制率、细胞凋亡以及对细胞黏附率的影响。方法:以霉酚酸酯在0.1μg/ml-100μg/ml,24-72h内作用于肝癌细胞,MTT法检测肿瘤细胞的生长抑制率,流式细胞仪检测细胞周期,Hoechst33258荧光染色观察细胞凋亡的形态变化,细胞黏附实验检测细胞黏附率的影响。结果:霉酚酸酯显著的抑制了肿瘤细胞的增长,并显著的抑制其黏附率,在浓度为100μg/ml作用72小时时生长抑制率达78.8%,黏附率降低至42.1%,Hoechst33258染色实验发现随浓度增大细胞凋亡的发生增多,核固缩、核碎裂的现象发生越明显。流式细胞仪检测,细胞周期阻滞于GO/G1期,减少增殖细胞在S期的分布。结论:霉酚酸酯对肝癌细胞HepG-2的增长具有明显的抑制作用。 | 刘屹 褚延魁 王成果 臧莉 杨媛 杜锡林 董瑞 宋舟 江雪 鲁建国 马庆久 | 2008 | 现代生物医学进展2008,8,3: | 0 |