期刊文献+

二次检索

题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

年份

学科

共找到26篇文章
< 1 2 >
每页显示 20 50 100
黄芩甙体外对人肝癌细胞BEL-7402的诱导分化作用 被引量:15
1
作者 郭霞 郭昱 《世界华人消化杂志》 CAS 北大核心 2008年第10期1119-1123,共5页
目的:探讨黄芩甙对人肝癌BEL-7402细胞系分化的影响.方法:应用细胞培养技术培养BEL-7402细胞,MTT实验和软琼脂克隆形成实验观察黄芩甙对肝癌细胞增殖的作用.光镜、电子显微镜观察细胞形态、超微结构,酶促反应试剂盒检测细胞浆中碱性磷酸... 目的:探讨黄芩甙对人肝癌BEL-7402细胞系分化的影响.方法:应用细胞培养技术培养BEL-7402细胞,MTT实验和软琼脂克隆形成实验观察黄芩甙对肝癌细胞增殖的作用.光镜、电子显微镜观察细胞形态、超微结构,酶促反应试剂盒检测细胞浆中碱性磷酸酶(ALP)、γ-谷氨酰转移酶(γ-GT)活性,放免法检测细胞甲胎蛋白(AFP)、白蛋白(ALB)分泌量和细胞内环核苷酸(cAMP)含量,流式细胞术测定细胞周期,免疫组化染色检测细胞AFP表达.结果:黄芩甙能明显抑制肝癌细胞增殖,对肝癌细胞形态及超微结构的观察显示黄芩甙作用后细胞趋于成熟分化,实验组AFP在胞质内均匀分布,呈黄色,着色较淡.黄芩甙作用后γ-GT比活力明显低于对照组(135±10nkat/gvs2432±15nkat/g,P<0.05),ALP比活力明显高于对照组(6635±1350nkat/gvs5872±450nkat/g,P<0.05),ALP耐热型同工酶即胎盘型ALP活性显著低于对照组,黄芩甙组AFP分泌量较对照组细胞显著性降低,ALB分泌显著升高,细胞内cAMP含量增加.随黄芩甙浓度的增加和作用时间的延长肝癌细胞G1/G0期比例逐步增高,S期细胞减少.结论:黄芩甙能诱导肝癌细胞分化,与细胞周期调节密切相关. 展开更多
关键词 黄芩甙能诱导肝癌细胞分化 与细胞周 期调节密切相关
下载PDF
二乙基亚硝胺诱导建立Apc基因突变大鼠与F344大鼠肝癌模型的比较 被引量:1
2
作者 谢蓓 赵磊 +3 位作者 孙婧 张丽娟 库本高志 魏虎来 《实验动物与比较医学》 CAS 2017年第3期191-197,共7页
目的采用二乙基亚硝胺(DEN)在F344大鼠、Kyoto Apc Delta(KAD)大鼠体内诱发制备肝癌模型,并比较其优劣。方法 KAD大鼠25只,随机法分组,阴性对照组(5只)给予正常饮水;DEN造模组(20只)前5周饮水中添加40μg/mL DEN,6~20周给予正常饮水;定... 目的采用二乙基亚硝胺(DEN)在F344大鼠、Kyoto Apc Delta(KAD)大鼠体内诱发制备肝癌模型,并比较其优劣。方法 KAD大鼠25只,随机法分组,阴性对照组(5只)给予正常饮水;DEN造模组(20只)前5周饮水中添加40μg/mL DEN,6~20周给予正常饮水;定期解剖大鼠,肉眼观察肝脏病变并取病变组织及癌旁组织制作病理切片。25只F344大鼠采用相同方法进行实验。结果F344大鼠和KAD大鼠均可成功诱发肝癌,且肝癌发生病理过程与人类相似。造模16周时KAD大鼠就可见灰白色病灶点,3/4大鼠成瘤,平均病灶数为1.00±0.82个;造模20周时,KAD大鼠全部(4/4)成瘤,病灶数为3.50±1.29个;而F344大鼠迟至20周时才可观察到类似病灶,3/4大鼠成瘤,病灶数为1.25±0.96个。KAD大鼠的诱导成瘤性显著高于亲代F344大鼠(P<0.05)。结论与亲代F344大鼠相比,抑癌基因Apc突变的KAD大鼠经DEN诱导更易发生肝癌,且该模型具有肝癌诱发时间短、相同诱导时间肝癌发生率高、诱发病灶数多等优点,是化学诱发制备肝癌动物模型的良好模式动物。 展开更多
关键词 KAD大鼠 F344大鼠 肝癌诱导 二乙基亚硝胺(DEN)
下载PDF
土贝母皂苷Ⅱ对诱导性肝癌大鼠肝细胞周期的影响
3
作者 晁旭 崔亚亚 +4 位作者 成晓 魏敏慧 党琳 史海龙 杨新捷 《中国中医急症》 2012年第6期923-923,941,共2页
目的观察土贝母皂苷Ⅱ对诱导性肝癌大鼠肝细胞周期的影响。方法以诱导性肝癌大鼠为材料,采用流式细胞仪检测土贝母皂苷Ⅱ对诱导性肝癌大鼠肝细胞DNA含量,并分析细胞周期。结果经土贝母皂苷Ⅱ治疗的动物肝S期细胞较模型组明显减少,而G1/G... 目的观察土贝母皂苷Ⅱ对诱导性肝癌大鼠肝细胞周期的影响。方法以诱导性肝癌大鼠为材料,采用流式细胞仪检测土贝母皂苷Ⅱ对诱导性肝癌大鼠肝细胞DNA含量,并分析细胞周期。结果经土贝母皂苷Ⅱ治疗的动物肝S期细胞较模型组明显减少,而G1/G0期细胞增多,几乎恢复到正常水平。结论土贝母皂苷Ⅱ可以阻止肝细胞从G1期向S期进程,使DNA合成受到抑制和阻断,造成G1期细胞的堆积。 展开更多
关键词 土贝母皂苷Ⅱ 诱导肝癌大鼠 细胞周期
下载PDF
Endostar对血管新生和肝癌诱导的血管新生的抑制作用 被引量:1
4
作者 叶庆 秦叔逵 殷晓进 《中国处方药》 2008年第9期81-81,共1页
目的:研究Endostar对血管新生的抑制作用和对肝癌细胞诱导的血管新生的抑制作用。
关键词 血管新生 肝癌诱导 抑制作用 荧光定量分析 HUVEC BOYDEN小室 试验研究 定量检测
下载PDF
三氧化二砷对肝癌诱导血管内皮细胞相关基因蛋白表达的影响 被引量:16
5
作者 崔永安 秦叔逵 +2 位作者 陈惠英 王锦鸿 左小东 《世界华人消化杂志》 CAS 北大核心 2005年第9期1142-1144,共3页
目的:研究三氧化二砷(As2O3)注射液对肝癌诱导血管内皮细胞相关基因蛋白表达的影响.方法:构建了人肝癌SMMC-7721细胞株诱导人脐静脉内皮细胞ECV304增殖的实验模型,应用免疫组织化学方法,严密观察了As2O3注射液对SMMC-7721细胞、ECV304... 目的:研究三氧化二砷(As2O3)注射液对肝癌诱导血管内皮细胞相关基因蛋白表达的影响.方法:构建了人肝癌SMMC-7721细胞株诱导人脐静脉内皮细胞ECV304增殖的实验模型,应用免疫组织化学方法,严密观察了As2O3注射液对SMMC-7721细胞、ECV304细胞及SMMC-7721细胞条件培养液培养的ECV304细胞,有关基因蛋白表达的影响.结果:2mg/L的As2O3注射液,对SMMC-7721细胞、ECV304细胞及SMMC-7721细胞条件培养液培养的ECV304细胞表达肿瘤相关基因蛋白,均有一定的调节作用;可下调VEGF、整合素β1和EGFR的表达;上调E-钙粘连蛋白的表达.结论:As2O3注射液抗原发性肝癌及防治肝癌复发和转移的作用机制,可能与其能调节肝癌细胞及血管内皮细胞VEGF、整合素β1、E-钙粘连蛋白和EGFR等基因蛋白的表达,干预细胞的信号转导,抑制肿瘤血管形成有关. 展开更多
关键词 相关基因蛋白表达 血管内皮细胞 三氧化二砷 肝癌诱导 肝癌SMMC-7721细胞株 As2O3注射液 ECV304细胞 人脐静脉内皮细胞 免疫组织化学方法 条件培养液 钙粘连蛋白 肿瘤血管形成 VEGF EGFR 原发性肝癌 整合素β1 实验模型
下载PDF
细胞色素P450酶在化学物质诱导肝脏癌变作用及研究现状
6
作者 刘琳琳 任进 《毒理学杂志》 CAS CSCD 北大核心 2004年第S1期313-317,共5页
关键词 细胞色素P450酶 化学物诱导肝癌 癌变早期
下载PDF
化学致癌物与肝癌的研究 被引量:3
7
作者 钱妍 俞超琴 《环境与健康杂志》 CAS CSSCI CSCD 北大核心 1999年第5期311-313,共3页
关键词 化学致癌物 肝癌防治 肝癌诱导
下载PDF
二乙基亚硝胺联合四氯化碳诱发C57BL/6小鼠肝癌模型 被引量:3
8
作者 仲鑫汝 许龙 +2 位作者 田睿 苏静 张勇 《中国比较医学杂志》 CAS 北大核心 2020年第1期12-16,共5页
目的通过建立C57BL/6小鼠化学诱发性肝癌模型模拟肝癌发生发展进程探索肝癌发生机制。方法选取110只C57BL/6小鼠,随机分为对照组(30只)和模型组(80只),对照组小鼠无处理,模型组通过灌胃给药CCl4联合腹腔注射DEN的方法建立肝癌模型;持续... 目的通过建立C57BL/6小鼠化学诱发性肝癌模型模拟肝癌发生发展进程探索肝癌发生机制。方法选取110只C57BL/6小鼠,随机分为对照组(30只)和模型组(80只),对照组小鼠无处理,模型组通过灌胃给药CCl4联合腹腔注射DEN的方法建立肝癌模型;持续测量小鼠体重,不同时间节点解剖小鼠观察肝形态、测定静脉血血清中肝功能相关酶的水平、观察肝组织病理学变化。结果与对照组相比,模型组小鼠体重逐渐降低,肝形态失常,血清中肝功能相关酶ALT、AST升高,有明显的肝癌组织病理学改变。结论二乙基亚硝胺(DEN)联合四氯化碳(CCl4)可诱发C57BL/6小鼠肝癌,为研究肝癌发生发展的分子机制提供可靠的动物模型。 展开更多
关键词 化学诱导肝癌模型 二乙基亚硝胺(DEN) 四氯化碳(CCl4) C57BL/6小鼠
下载PDF
健脾化瘀方对人肝癌细胞SMMC-7721增殖和凋亡的影响 被引量:5
9
作者 赵江 王瑞平 邹玺 《实用中医内科杂志》 2009年第11期30-31,33,共3页
[目的]探讨健脾化瘀方对人肝癌细胞系SMMC-7721的抑制率及药物浓度和作用时间对细胞抑制率的影响,以及IC_(50)药物浓度下对SMMC-7721凋亡的影响。[方法]采用MTT法,观察不同浓度的健脾化瘀方对人肝癌细胞株SMMC-7721增殖的影响及与药物... [目的]探讨健脾化瘀方对人肝癌细胞系SMMC-7721的抑制率及药物浓度和作用时间对细胞抑制率的影响,以及IC_(50)药物浓度下对SMMC-7721凋亡的影响。[方法]采用MTT法,观察不同浓度的健脾化瘀方对人肝癌细胞株SMMC-7721增殖的影响及与药物作用时间之间的关系。用AnnexinV/PI双染色法,用流式细胞仪检测健脾化瘀方对肝癌细胞株SMMC-7721凋亡的影响。[结果]健脾化瘀方浓度在5mg/mL时,对SMMC-7721细胞的增殖有明显的抑制作用,呈剂量依赖和时间依赖效应关系。健脾化瘀方对人肝癌细胞SMMC-7721作用24h后,肝癌细胞凋亡率升高,并有一定的浓度依赖性。[结论]健脾化瘀方有抑制SMMC-7721细胞的增殖,能诱导人肝癌细胞株SMMC-7721的凋亡。 展开更多
关键词 健脾 化瘀方 诱导肝癌细胞株 SMMC-7721细胞 增殖和凋亡 Hepatocellular Carcinoma Cell 药物浓度 作用时间 细胞抑制率 流式细胞仪检测 肝癌细胞系 细胞凋亡率 浓度依赖性 抑制作用 效应关系 双染色法 时间依赖 剂量依赖 不同浓度 MTT法
下载PDF
去唾液酸糖蛋白受体(ASGPR)在N-二硝基亚乙胺诱导原位肝癌模型、原位移植肝癌模型大鼠体内的表达与分布
10
作者 杨文川 张发斌 +3 位作者 胡春晖 孔宪梅 都涛 赵振文 《药物评价研究》 CAS 北大核心 2024年第2期302-308,共7页
目的 测定去唾液酸糖蛋白受体(ASGPR)在N-二硝基亚乙胺(DEN)诱导大鼠原位肝癌模型(DEN-HCC-Rat)和原位移植大鼠肝癌模型(OTT-HCC-Rat)中的表达。方法 DEN-HCC-Rat造模:模型组SD大鼠按照20 mg·kg^(-1) ig 0.25%DEN水溶液,每周1次,0.... 目的 测定去唾液酸糖蛋白受体(ASGPR)在N-二硝基亚乙胺(DEN)诱导大鼠原位肝癌模型(DEN-HCC-Rat)和原位移植大鼠肝癌模型(OTT-HCC-Rat)中的表达。方法 DEN-HCC-Rat造模:模型组SD大鼠按照20 mg·kg^(-1) ig 0.25%DEN水溶液,每周1次,0.025%DEN水溶液供动物饮用;对照组每周ig 1次0.9%氯化钠溶液,灭菌水供动物饮用,于造模第4、10、18、22周取材。OTT-HCC-Rat造模:模型组SD大鼠肝叶注射N1-S1细胞,假手术组大鼠麻醉后给予微创缝合处理,于注射后14 d取材。HE染色观察肝组织病变;通过免疫组化、免疫荧光、Western blotting和实时荧光定量PCR(qRT-PCR)实验检测各组ASGPR表达及分布。结果 通过HE染色确定DEN-HCC-Rat和OTT-HCC-Rat造模成功。在DEN-HCC-Rat中,免疫组化、免疫荧光、Western blotting、qRT-PCR结果均显示,与对照组比较,模型组大鼠肝组织ASGPR表达显著上调(P<0.05、0.01),且呈时间相关性;在OTT-HCC-Rat中,免疫组化结果显示模型组ASGPR表达显著高于假手术组(P<0.05),免疫荧光、Western blotting、qRT-PCR结果显示ASGPR在模型组与假手术组之间无显著性差异。结论DEN-HCC-Rat模型更好地模拟肿瘤微环境改变,且ASGPR在肝癌区域表达高于对照组大鼠肝脏,故可利用ASGPR介导肝靶向制剂的转运,提高肝靶向药物治疗效果。 展开更多
关键词 去唾液酸糖蛋白受体 N-二硝基亚乙胺 大鼠诱导原位肝癌模型 大鼠移植肝癌模型 靶向
原文传递
大鼠慢性压迫性脊髓损伤后EphA2在脊髓前角运动神经元中的表达 被引量:2
11
作者 裴有智 康学文 汪玉良 《兰州大学学报(医学版)》 CAS 2008年第3期35-38,共4页
目的探讨慢性脊髓损伤后红细胞生成素诱导肝癌细胞株受体A2(EphA2)在脊髓中的变化规律,寻找脊髓损伤后治疗的靶点。方法将40只Wistar大鼠分为假手术组、轻度压迫组(CR 20%)、中度压迫组(CR 40%)、重度压迫组(CR 60%)4组。T_(10)水平脊... 目的探讨慢性脊髓损伤后红细胞生成素诱导肝癌细胞株受体A2(EphA2)在脊髓中的变化规律,寻找脊髓损伤后治疗的靶点。方法将40只Wistar大鼠分为假手术组、轻度压迫组(CR 20%)、中度压迫组(CR 40%)、重度压迫组(CR 60%)4组。T_(10)水平脊髓背侧加压,压迫方法采用塑料螺钉渐进性加压,分次完成手术。对大鼠进行后肢运动功能评分及所取脊髓标本进行原位杂交分析,对脊髓前角EphA2阳性细胞率进行统计分析,比较各组之间的差异。结果EphA2阳性细胞主要存在于压迫远端脊髓灰质中,其中以脊髓前角运动神经元为著。假手术组有很少量EphA2阳性细胞,压迫组EphA2阳性细胞明显升高(P<0.01),中度压迫组及重度压迫组较轻度压迫组升高(P<0.05),中度压迫组及重度压迫组间差异无统计学意义(P>0.05)。结论慢性压迫性脊髓损伤后脊髓前角运动神经元EphA2表达升高。慢性脊髓压迫可以诱发脊髓EphA2表达升高,对脊髓损伤是一个保护性因素。 展开更多
关键词 慢性压迫性脊髓损伤 红细胞生成素诱导肝癌细胞株受体A2 原位杂交
下载PDF
Ascorbic Acid Promotes Arsenic-induced Cytotoxicity in Human Hepatocarcinoma Cells and Their Underlying Mechanisms
12
作者 吴辉文 吴向阳 陈锡慰 《Journal of Nanjing Medical University》 2004年第6期297-300,共4页
Objective: To study synergistic effect with Ascorbic acid(AA) on arsenic trioxide inducing human Hepatocarcinoma cell apoptosis, and provide theoretical basis for promoting human Hepatocarcinoma cell apoptosis induced... Objective: To study synergistic effect with Ascorbic acid(AA) on arsenic trioxide inducing human Hepatocarcinoma cell apoptosis, and provide theoretical basis for promoting human Hepatocarcinoma cell apoptosis induced by arsenic trioxide(AT). Methods: Human Hepatocarcinoma cell line BEL-7402 being cultured in vitro, the effect of AT and (or) AA on its growth inhibition and its two intracellular signal molecules was evaluated separately using MTT and Western blot. Results: AT at a few μmol/L concentration could suppress abnormal proliferation of human hepatocarcinoma cells, and initiate their apoptosis by activation of caspase-3, and activate extracellular-signal regulated kinases (ERKs), which were dependent on the dosage of AT conspicuously. The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs. Conclusion: Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERKs. 展开更多
关键词 HEPATOCARCINOMA arsenic trioxide Ascorbic acid apoptosis CASPASE-3 extracellular-signal regulated kinases
下载PDF
艾迪注射液对DEN诱导型肝癌大鼠体内细胞色素P450酶表达的影响 被引量:7
13
作者 朱晓青 陆苑 +4 位作者 刘亭 潘洁 刘春花 李勇军 王永林 《中国实验方剂学杂志》 CAS CSCD 北大核心 2021年第8期43-49,共7页
目的:观察艾迪注射液(AD)对二乙基亚硝胺(DEN)化学诱导的原发性肝癌(HCC)大鼠体内细胞色素P450(CYP450)4种亚型酶CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA和蛋白表达的影响。方法:健康SD雄大鼠随机选取3只作为空白组,余下大鼠采用DEN间断性... 目的:观察艾迪注射液(AD)对二乙基亚硝胺(DEN)化学诱导的原发性肝癌(HCC)大鼠体内细胞色素P450(CYP450)4种亚型酶CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA和蛋白表达的影响。方法:健康SD雄大鼠随机选取3只作为空白组,余下大鼠采用DEN间断性诱导原发性肝癌大鼠模型,模型成功后随机将大鼠分为模型组,AD组,每组3只。正常组与模型组腹腔注射10 mL·kg^(-1)生理盐水,AD组腹腔注射10 mL·kg^(-1)AD,1次/d,共干预14 d。采用实时荧光定量聚合酶链式反应(Real-time PCR)和蛋白免疫印迹法(Western blot)分别检测CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA和蛋白的表达。结果:Real-time PCR结果表明,给药14 d,与正常组比较,模型组大鼠癌旁组织(PCT)和癌灶组织(CT)CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA表达均明显下调(P<0.05,P<0.01);与模型组比较,AD组PCT中4种亚型酶mRNA表达明显下调(P<0.05,P<0.01),CT中4种亚型酶mRNA表达明显上调(P<0.05)。Western blot结果表明,与正常组比较,模型组CT中CYP1A2,CYP2E1,CYP3A2,CYP2C11蛋白表达均显著下调(P<0.01),PCT中CYP3A2,CYP2C11蛋白表达显著下调(P<0.01);与模型组比较,AD组CT,PCT中CYP1A2,CYP2E1,CYP3A2,CYP2C11蛋白表达有下调趋势,差异无统计学意义。结论:AD可下调大鼠肝组织中CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA和蛋白的表达。临床使用AD时,应注意可能因CYP450酶抑制引起的药物相互作用。 展开更多
关键词 艾迪注射液 诱导肝癌 二乙基亚硝胺 细胞色素P450 蛋白 mRNA
原文传递
Antitumor activities of human autologous cytokineinduced killer(CIK)cells against hepatocellular carcinoma cells in vitro and in vivo 被引量:107
14
作者 Fu-Sheng Wang Ming-Xu Liu Bing Zhang Ming Shi Zhou-Yun Lei Wen-Bing Sun Qing-You Du Ju-Mei Chen,Division of Biological Engineering,Beijing Institute of Infectious Diseases,Beijing 100039,China Wen-Bing Sun,Department of Surgery,Beijing Hospital of Infectious Diseases,Beijing 100039,China 《World Journal of Gastroenterology》 SCIE CAS CSCD 2002年第3期464-468,共5页
AIM: To characterize the anticancer function of cytokine-induced killer cells (CIK) and develop an adoptive immunotherapy for the patients with primary hepatocellular carcinoma (HCC), we evaluated the proliferation ra... AIM: To characterize the anticancer function of cytokine-induced killer cells (CIK) and develop an adoptive immunotherapy for the patients with primary hepatocellular carcinoma (HCC), we evaluated the proliferation rate, phenotype and the antitumor activity of human CIK cells from healthy donors and HCC patients in vitro and in vivo. METHODS: Peripheral blood mononuclear cells (PBMC) from healthy donors and patients with primary HCC were incubated in vitro and induced into CIK cells in the presence of various cytokines such as interferon-gamma (IFN-gamma), interleukin-1 (IL-1), IL-2 and monoclonal antibody (mAb) against CD3. The phenotype and characterization of CIK cells were identified by flow cytometric analysis. The cytotoxicity of CIK cells was determined by (51)Cr release assay. RESULTS: The CIK cells were shown to be a heterogeneous population with different cellular phenotypes. The percentage of CD3+/CD56+ positive cells, the dominant effector cells, in total CIK cells from healthy donors and HCC patients, significantly increased from 0.1-0.13% at day 0 to 19.0-20.5% at day 21 incubation, which suggested that the CD3+ CD56+ positive cells proliferated faster than other cell populations of CIK cells in the protocol used in this study. After 28 day in vitro incubation, the CIK cells from patients with HCC and healthy donors increased by more than 300-fold and 500-fold in proliferation cell number, respectively. CIK cells originated from HCC patients possessed a higher in vitro antitumor cytotoxic activity on autologous HCC cells than the autologous lymphokine-activated killer (LAK) cells and PBMC cells. In in vivo animal experiment, CIK cells had stronger effects on the inhibition of tumor growth in Balb/c nude mice bearing BEL-7402-producing tumor than LAK cells (mean inhibitory rate, 84.7% vs 52.8%, P【0.05) or PBMC (mean inhibitory rate, 84.7% vs 37.1%, P【0.01). CONCLUSION: Autologous CIK cells are of highly efficient cytotoxic effector cells against primary hepatocellular carcinoma cells and might serve as an alternative adoptive therapeutic strategy for HCC patients. 展开更多
关键词 Animals Carcinoma Hepatocellular Cell Division Cytokines Cytotoxicity Immunologic Humans IMMUNOPHENOTYPING Immunotherapy Adoptive Killer Cells Liver Neoplasms MICE Mice Nude Neoplasm Transplantation Research Support Non-U.S. Gov't Transplantation Heterologous Tumor Cells Cultured
下载PDF
Induction of apoptosis and cell cycle arrest in human HCC MHCC97H cells with Chrysanthemum indicum extract 被引量:7
15
作者 Zong-Fang Li Zhi-Dong Wang +4 位作者 Yuan-Yuan Ji Shu Zhang Chen Huang Jun Li Xian-Ming Xia 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第36期4538-4546,共9页
AIM: To investigate the effects of Chrysanthemum indicum extract (CIE) on inhibition of proliferation and on apoptosis, and the underlying mechanisms, in a human hepatocellular carcinoma (HCC) MHCC97H cell line. ... AIM: To investigate the effects of Chrysanthemum indicum extract (CIE) on inhibition of proliferation and on apoptosis, and the underlying mechanisms, in a human hepatocellular carcinoma (HCC) MHCC97H cell line. METHODS: Viable rat hepatocytes and human endothelial ECV304 cells were examined by trypan blue exclusion and MTT assay, respectively, as normal controls. The proliferation of MHCC97H cells was determined by MTT assay. The cellular morphology of MHCC97H cells was observed by phase contrast microscopy. Flow cytometry was performed to analyze cell apoptosis with annexin V/propidium iodide (PI), mitochondrial membrane potential with rhodamine 123 and cell cycle with PI in MHCC97H cells. Apoptotic proteins such as cytochrome C, caspase-9, caspase-3 and cell cycle proteins, including P21 and CDK4, were measured by Western blotting. RESULTS: CIE inhibited proliferation of MHCC97H cells in a timeand dose-dependent manner without cytotoxicity in rat hepatocytes and human endothelial ceils. CIE induced apoptosis of MHCC97H cells in a concentration-dependent manner, as determined by flow cytometry. The apoptosis was accompanied by a decrease in mitochondrial membrane potential, release of cytochrome C and activation of caspase-9 and caspase-3. CIE arrested the cell cycle in the S phase by increasing P21 and decreasing CDK4 protein expression. CONCLUSION: CIE exerted a significant apoptotic effect through a mitochondrial pathway and arrested the cell cycle by regulation of cell cycle-related proteins in MHCC97H cells without an effect on normal cells. The cancer-specific selectivity shown in this study suggests that the plant extract could be a promising novel treatment for human cancer. 展开更多
关键词 APOPTOSIS Cell cycle Chinese traditionalmedicine Chrysanthemum indicum Hepatocellularcarcinoma Herbal medicine
下载PDF
Octreotide induces caspase activation and apoptosis in human hepatoma HepG2 cells 被引量:5
16
作者 Nikos J Tsagarakis Ioannis Drygiannakis +2 位作者 Antonis G Batistakis George Kolios Elias A Kouroumalis 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第3期313-321,共9页
AIM: To investigate the role of octreotide on cellular proliferation and apoptosis of human hepatoma (HepG2) cells. METHODS: We studied cellular proliferation, apoptosis and the possible internal caspase-mediated apop... AIM: To investigate the role of octreotide on cellular proliferation and apoptosis of human hepatoma (HepG2) cells. METHODS: We studied cellular proliferation, apoptosis and the possible internal caspase-mediated apoptosis pathway involved, after treatment of HepG2 carcinoma cells with octreotide in comparison with the apoptosis caused by tumor necrosis factor-α (TNF-α). Activities of caspase-3, caspase-9, caspase-8 and caspase-2 were studied, while apoptosis was investigated through detection of DNA fragmentation and through identification of apoptotic cells with the annexin-V/propidium iodide flow cytometric method. RESULTS: After an initial increase in HepG2 cellular proliferation, a significant inhibition was observed with 10-8 mol/L octreotide, while TNF-α dose-dependently decreased proliferation. Early and late apoptosis was significantly increased with both substances. Octreotide significantly increased caspase-3, caspase-8 and caspase-2 activity. TNF-α signifi cantly increased only caspase-2. Cellular proliferation was decreased after treatment with octreotide or TNF-α alone but, in contrast to TNF-α, octreotide decreased proliferation only at concentrations of 10-8 mol/L, while lower concentrations increased proliferation. CONCLUSION: Our findings are suggestive of caspasemediated signaling pathways of octreotide antitumor activity in HepG2 cells, and indicate that measurements of serum octreotide levels may be important, at least in clinical trials, to verify optimal therapeutic drug concentrations. 展开更多
关键词 OCTREOTIDE Hepatocellular carcinoma APOPTOSIS CASPASES SOMATOSTATIN
下载PDF
Tea pigments induce cell-cycle arrest and apoptosis in HepG2 cells 被引量:2
17
作者 Xu-Dong Jia Chi Han Jun-Shi Chen 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第34期5273-5276,共4页
AIM: To investigate the molecular mechanisms by which tea pigments exert preventive effects on liver carcinogenesis. METHODS: HepG2 cells were seeded at a density of 5×10^5/well in six-well culture dishes and i... AIM: To investigate the molecular mechanisms by which tea pigments exert preventive effects on liver carcinogenesis. METHODS: HepG2 cells were seeded at a density of 5×10^5/well in six-well culture dishes and incubated overnight. The cells then were treated with various concentrations of tea pigments over 3 d, harvested by trypsinization, and counted using a hemocytometer. Flow cytometric analysis was performed by a flow cytometer after propidium iodide labeling. Bd-2 and p21^WAF1 proteins were determined by Western blotting. In addition, DNA laddering assay was performed on treated and untreated cultured HepG2 cells. RESULTS: Tea pigments inhibited the growth of HepG2 cells in a dose-dependent manner. Flow-cytometric analysis showed that tea pigments arrested cell cycle progression at G1 phase. DNA laddering was used to investigate apoptotic cell death, and the result showed that 100 mg/L of tea pigments caused typical DNA laddering. Our study also showed that tea pigments induced upregulation of p21^WAF1 protein and downregulation of Bcl-2 protein. CONCLUSION: Tea pigments induce cell-cycle arrest and apoptosis. Tea pigments may be used as an ideal chemopreventive agent. 展开更多
关键词 Tea pigments Cell cycle APOPTOSIS
下载PDF
Knockdown of survivin gene expression by RNAi induces apoptosis in human hepatocellular carcinoma cell line SMMC-7721 被引量:42
18
作者 Sheng-QuanCheng Wen-LiangWang +3 位作者 WeiYan Qing-LongLi LiWang Wen-YongWang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第5期756-759,共4页
AIM: To investigate the survivin gene expression in human hepatocellular carcinoma cell line SMMC-7721 and the effects of survivin gene RNA interference (RNAi) on cell apoptosis and biological behaviors of SMMC-7721 c... AIM: To investigate the survivin gene expression in human hepatocellular carcinoma cell line SMMC-7721 and the effects of survivin gene RNA interference (RNAi) on cell apoptosis and biological behaviors of SMMC-7721 cells. METHODS: Eukaryotic expression vector of survivin gene RNAi and recombinant plasmid pSuppressorNeo-survivin (pSuNeo-SW), were constructed by ligating into the vector, pSupperssorNeo (pSuNeo) digested with restriction enzymes Xba I and Sail and the designed double-chain RNAi primers. A cell model of SMMC-7721 after treatment with RNAi was prepared by transfecting SMMC-7721 cells with the lipofectin transfection method. Strept-avidin-biotin-complex (SABC) immunohistochemical staining and RT-PCR were used to detect survivin gene expressions in SMMC-7721 cells. Flow cytometry was used for the cell cycle analysis. Transmission electron microscopy was performed to determine whether RNAi induced cell apoptosis, and the method of measuring the cell growth curve was utilized to study the growth of SMMC-7721 cells before and after treatment with RNAi. RESULTS: The eukaryotic expression vector of survivin gene RNAi and pSuNeo-SW, were constructed successfully. The expression level of survivin gene in SMMC-7721 cells was observed. After the treatment of RNAi, the expression of survivin gene in SMMC-7721 cells was almost absent, apoptosis index was increased by 15.6%, and the number of cells was decreased in G2/M phase and the cell growth was inhibited. CONCLUSION: RNAi can exert a knockdown of survivin gene expression in SMMC-7721 cells, and induce apoptosis and inhibit the growth of carcinoma cells. 展开更多
关键词 Hepatocellular carcinoma Survivin RNA interference APOPTOSIS Gene expression
下载PDF
p28^GANK inhibits endoplasmic reticulum stress-induced cell death via enhancement of the endoplasmic reticulum adaptive capacity 被引量:14
19
作者 Rong-Yang Dai Yao Chen +8 位作者 Jing Fu Li-Wei Dong Yi-Bin Ren Guang-Zhen Yang You-Wen Qian Jie Cao Shan-Hua Tang Sheng-Li Yang Hong-Yang Wang 《Cell Research》 SCIE CAS CSCD 2009年第11期1243-1257,共15页
It has been shown that oncoprotein p28GANK, which is consistently overexpressed in human hepatocellular carcinoma (HCC), plays a critical role in tumorigenesis of HCC. However, the underlying mechanism remains uncle... It has been shown that oncoprotein p28GANK, which is consistently overexpressed in human hepatocellular carcinoma (HCC), plays a critical role in tumorigenesis of HCC. However, the underlying mechanism remains unclear. Here, we demonstrated that p28GANK inhibits apoptosis in HCC cells induced by the endoplasmic reticulum (ER) stress. During ER stress, p28GANK enhances the unfolded protein response, promotes ER recovery from translational repression, and thereby facilitates cell's ability to cope with the stress conditions. Furthermore, p28GANK upregulates glucose-regulated protein 78 (GRP78), a key ER chaperone protein, which subsequently enhances the ER folding capacity and promotes recovery from ER stress. We also demonstrated that p28GANK increases p38 mitogen-activated protein kinase and Akt phosphorylation, and inhibits nuclear factor kappa B (NF-κB) activation under ER stress, which in turn contributes to GRP78 upregulation. Taken together, our results indicate that p28GANK inhibits ER stress-induced apoptosis in HCC cells, at least in part, by enhancing the adaptive response and GRP78 expression. We propose that p28GANK has potential implications for HCC progression under the ER stress conditions. 展开更多
关键词 p28GANK ER stress UPR GRP78 APOPTOSIS
下载PDF
Abnormal expression of hypoxia inducible factor-1α and clinical values of molecular-targeted interference in hepatocellular carcinoma
20
作者 Shanshan Li Dengfu Yao +6 位作者 Zhizhen Dong Yajie Qian Dandan Yu Ninghua Yao Jie Chen Xiaodi Yan Chenglin Qin 《The Chinese-German Journal of Clinical Oncology》 CAS 2012年第3期125-129,共5页
Objective:The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells.Methods:HIF-1α expres... Objective:The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells.Methods:HIF-1α expression was analyzed in the self-control HCC specimens by immunohistochemistry.After HepG2 cells with miRNA transfection,the expression of HIF-1α was determined at mRNA or protein level by real-time polymerase chain reaction (PCR) or Western blotting.Vascular endothelial growth factor (VEGF) and angiopoietin-2 (ANG-2) were determined by ELISA.Alterations of cell cycles and apoptosis of HepG2 cells were measured using a flow cytometer.Results:Positive HIF-1α was brown and granule-like in the cytoplasm or nucleus.Significant difference was found between HCC (80%) and its surrounding tissues (100%,χ2=22.35,P < 0.001) and HIF-1α expression related to tumor size.At 72 h after miRNA transfection,the expression of HIF-1α in HepG2 cells was down-regulated by 87% at mRNA or 65% at protein level,with VEGF and ANG-2 decreased to 54% and 36%,respectively.After RNA interference combined with anti-cancer drug,the apoptotic rate of HepG2 cells was increasing from 22.46% ± 0.61% to 36.99% ± 0.88%,with up-regulation of G1 phase (65.68% ± 0.91%) and down-regulation of S phase (19.47 ± 1.34 %).Conclusion:Abnormal expression of HIF-1α is associated with development of HCC,and HIF-1α gene silencing can effectively inhibit HepG2 cell proliferation. 展开更多
关键词 hepatocellular carcinoma (HCC) hypoxia inducible factor-1α (HIF-1α) EXPRESSION RNA interference gene silencing
下载PDF
上一页 1 2 下一页 到第
使用帮助 返回顶部