藤梨根提取物对大肠癌LoVo细胞增殖的抑制作用及诱导凋亡的影响

目的:研究藤梨根提取物(ethanol extract from radix of actinidia chinensis,EERAC)对人大肠癌LoVo细胞增殖和凋亡的影响.方法:提取藤梨根抗癌有效活性成分(EERAC),按浓度分为4处理组(10、40、160、320mg/L)和空白对照组(0mg/L).各实验组经作用24、48、72h后,进行一般形态学和AO/EB荧光染色观察;MMT法检测细胞增殖的抑制情况;免疫组织化学(immunohistochemistry,IHC)法测定LoVo细胞中凋亡相关基因Bcl-2、Bax、Caspase-3的蛋白表达变化.结果:与空白对照组比较,一般形态学显示EERAC处理组能使细胞密度减低,增殖变慢;细胞逐渐变大,细胞间接触变松,胞浆中颗粒增多,细胞脱壁现象和周围碎片增多;荧光染色观察可见处理组细胞呈橙红色荧光,细胞核出现碎片状或固缩状的凋亡特征学形态改变,凋亡现象与EERAC的浓度呈正相关性;MTT法检测显示,EERAC处理组对LoVo细胞的最佳作用时间为72h,最大抑制率为79.48%,具有浓度和时间的依赖性(P<0.01);IHC检测结果显示EERAC作用LoVo细胞24h后,Bcl-2表达明显减弱,Bax、Caspase-3表达水平明显增高,Bcl-2/Bax比值下降,差异具有统计学意义(P<0.05),其效应与浓度相关.结论:EERAC具有明显抑制LoVo细胞增殖的作用,其机制可能与降低Bcl-2表达,上调Bax、Caspase-3的表达水平,激活线粒体凋亡途径有关.     

罗格列酮在人结肠癌氟尿嘧啶化疗增敏作用中对细胞凋亡的影响

目的 探讨过氧化物酶体增殖因子活化受体γ(peroxisome proliferator-activated receptor gammar,PPARγ)配体罗格列酮对人结肠癌氟尿嘧啶化疗增敏作用中细胞凋亡的影响.方法 体外培养人结肠癌HT-29细胞,分别或联合应用不同浓度的罗格列酮、氟尿嘧啶(fluorouracil,5-Fu)处理HT-29细胞,PI染色流式细胞术(FCM)分析、吖啶橙/溴乙啶(AO/EB)荧光染色法观察细胞凋亡率.用Western印迹法检测HT-29细胞PPARγ、NF-κB、Bcl-2、Bax的表达.结果 (1)流式细胞术和AO/EB荧光双染色法结果显示:5-Fu能明显诱导HT-29细胞凋亡,呈剂量依赖性.3.0,6.0,12.0 μg/L处理HT-29细胞72 h,细胞凋亡率分别为13.91%,18.16%,23.14%,罗格列酮亦能诱导HT-29细胞凋亡,呈剂量依赖性.1.0,10.0,100.0 μmol/L罗格列酮处理HT-29细胞72 h后,细胞凋亡率分别为1.44%,2.34%,14.13%.无细胞毒浓度的罗格列酮能显著促进5-Fu诱导HT-29细胞凋亡.1.0 μmol/L罗格列酮与12.0 μg/L 5-Fu合用使HT-29细胞凋亡率高达48.41%.(2)Werstern印迹法结果显示HT-29细胞表达PPARγ,罗格列酮作用HT-29细胞后上调PPARγ和Bax蛋白的表达,下调NF-κB、Bcl-2蛋白的表达,且呈浓度依赖方式(P<0.05).结论 (1)无细胞毒浓度下(1.0 μmol/L)罗格列酮能促进5-Fu诱导HT-29细胞凋亡.(2)罗格列酮的化疗增敏作用中对细胞凋亡的影响可能与活化PPARγ,下调NF-κB、Bcl-2蛋白表达,上调Bax蛋白表达有关.     

瑞香狼毒药效组分对裸鼠肝癌移植瘤的抑制及其机制

目的:评价瑞香狼毒药效组分抑制人肝癌细胞株BEL-7402裸鼠皮下移植瘤作用的强度,并探讨其机制.方法:建立人肝癌BEL-7402裸小鼠皮下移植瘤模型研究瑞香狼毒药效组分Zp1111抗肿瘤作用与对荷瘤裸鼠体质量与免疫器官的影响,免疫组织化学法检测用药前后BEL-7402皮下移植瘤组织Bcl-2与Bax阳性表达的变化.结果:Zp1111对裸小鼠皮下移植瘤BEL-7402具有较强的抑制作用,187.5mg/kg、250mg/kg(折合成生药量)剂量时对移植瘤的相对肿瘤增殖率T/C小于60%;该组分能显著上调BEL-7402移植瘤组织Bax基因的表达,但对Bcl-2的表达影响较弱.结论:瑞香狼毒药效组分在体内对人肝癌细胞BEL-7402裸鼠移植瘤具有较强的抑制作用并呈现一定的剂量依赖关系,该组分具有一定的诱导凋亡作用,可能与上调Bax有关.     

丹皮酚对人大肠癌HT-29细胞增殖、凋亡的影响及其分子机制

目的:探讨丹皮酚(paeonol, Pae)对人大肠癌HT-29细胞的增殖抑制、凋亡诱导作用及可能的作用机制. 方法:应用MTT法、荧光显微镜及透射电镜技术、TUNEL法和流式细胞仪技术观察不同浓度的Pae对HT-29细胞增殖的抑制及凋亡的诱导作用; 应用免疫细胞化学技术检测用药前后凋亡相关基因Bcl-2, Bax及P53表达的变化. 结果: HT-29细胞经Pae(浓度范围7.81-250 mg/L)作用后细胞生长明显受到抑制, 呈明显的剂量依赖效应关系和时间依赖效应关系; 荧光显微镜及透射电镜观察到Pae作用后HT-29细胞出现典型的细胞凋亡形态; Pae在15.63, 62.5, 250 mg/L 3种浓度下作用48 h均可诱导HT-29细胞凋亡, TUNEL法显示凋亡指数与Pae浓度呈正相依赖关系; 流式细胞仪技术检测其凋亡率分别为7.6%, 16.2%和34.5%, 也有明显的剂量效应关系, 同时Pae使细胞周期分布发生明显变化, 表现为S期细胞比例上升, G0/G1期和G2/M期细胞比例下降; 免疫细胞化学结果显示Pae作用后HT-29细胞Bcl-2及P53蛋白表达显著降低, Bax蛋白表达无显著改变. 结论:Pae能抑制HT-29细胞增殖并诱导其凋亡, 呈现明显的剂量依赖效应关系和时间依赖效应关系. 其作用可能与影响癌细胞的细胞周期、下调Bcl-2/Bax的比例及P53蛋白的表达有关.     

参麦注射液对LWEIS肺癌小鼠的抗肿瘤及作用机制研究

目的研究参麦注射液对Lweis肺癌小鼠的抗肿瘤作用。方法建立Lweis细胞小鼠移植瘤模型,将荷瘤小鼠随机分为荷瘤对照组,阳性对照组及参麦注射液三个剂量组,另设正常对照组,每日灌胃给药,通过测定抑瘤率,脾脏指数,胸腺指数,TNF-α、Bcl-2、Bax、caspase-9含量,探讨参麦注射液的抗肿瘤作用及作用机制。结果参麦注射液抑制Lweis肺癌小鼠瘤块的生长,降低荷瘤小鼠的脾脏指数,胸腺指数,促进TNF-α,Bax和Caspase-9生成,抑制Bcl-2含量。结论参麦注射液可通过增强荷瘤机体免疫功能及诱导凋亡而发挥抗肿瘤作用。     

罗格列酮对人结肠癌裸鼠移植瘤生长作用研究

目的观察过氧化物酶体增殖物激活受体的配体罗格列酮（ROZ）对人结肠癌细胞系HT-29裸鼠移植瘤的作用,探讨ROZ活化PPARγ,下调NFκB,从而诱导人结肠癌细胞凋亡的作用机制。方法体外培养人结肠癌HT-29细胞,建立人结肠癌细胞HT-29裸鼠移植瘤模型,20只荷瘤裸鼠随机分组进行实验。Western Blot法分析PPARγ、NF-κB、Bcl-2、bax蛋白表达的影响及PPARγ活化依赖性。结果 ROZ能抑制裸鼠移植瘤的生长。结论 ROZ通过上调PPARγ蛋白表达,下调NF-κB蛋白表达,抑制人结肠癌裸鼠移植瘤生长。     

芹菜素与老年大鼠缺血心肌细胞凋亡及Bcl-2、Bax、Caspase-3表达的相关性

目的对芹菜素与老年大鼠缺血心肌细胞凋亡及Bcl-2、Bax、半胱天冬酶(Caspase)-3表达相关性进行研究。方法选取选择健康的老年大鼠60只,随机分为正常组、假手术组、心肌缺血再灌注组和不同剂量芹菜素组各10只。制作缺血再灌注模型采用结扎左冠状勤脉前降支,心肌缺血30 min,再灌注2 h。假手术组只穿线不结扎,余各组在缺血前10 min股静脉分别注射生理盐水、聚乙二醇、低剂量、中剂量、高剂量芹菜素,检测缺血心肌细胞凋亡及Bcl-2、Bax、Caspase-3表达。结果正常组和假手术组的凋亡细胞数极少;心肌缺血再灌注组的凋亡细胞数量明显的增多,芹菜素低剂量(1 mg/kg)组:Apil1、芹菜素中剂量(2 mg/kg)组:Apil2、芹菜素高剂量(4 mg/kg)组:Apil4的凋亡的凋亡细胞数下降,其中芹菜素高剂量(4 mg/kg)组:Apil4的凋亡细胞数下降明显。心肌缺血再灌注组的Bcl-2、Bax、Caspase-3、AR与正常组、假手术组、芹菜素高、中、低剂量组比较,差异有统计学意义(P<0.05)。芹菜素低剂量组Bcl-2、Bax、Caspase-3、AR与正常组、假手术组、心肌缺血再灌注组、芹菜素高剂量组比较,差异有统计学意义(P<0.05)。芹菜素中剂量组Bcl-2、Bax、Caspase-3、AR与正常组、假手术组、心肌缺血再灌注组、芹菜素高剂量组比较,差异有统计学意义(P<0.05)。且芹菜素低剂量组的Bax、AR与芹菜素中剂量组比较,差异有统计学意义(P<0.05)。结论芹菜素与缺血心肌细胞凋亡及Bcl-2、Bax、Caspase-3表达存在相关性,且芹菜素可以减轻心肌损伤。     

过表达miR-150通过PI3K/AKT信号通路调控结直肠癌细胞凋亡的机制研究

目的探讨过表达miR-150通过磷脂酰肌醇-3-羟激酶/丝苏氨酸蛋白激酶(phosphatidylinositol 3-hydroxykinase/seronine kinase,PI3K/AKT)信号通路调控结直肠癌细胞凋亡的机制。方法将体外培养HT-29细胞分为空白对照组(转染空脂质体) NC组(转染mimic)和miR-150(转染miR-150 mimic);采用RT-PCR检测转染后细胞中miR-150 mRNA水平; CCK-8法检测细胞增殖;流式细胞仪检测细胞凋亡; WB法检测Cleaved caspase3、PI3K、p-PI3K、AKT、p-AKT蛋白表达。将对数生长期HT-29分为阴性对照组、miR-150组、LY294002组和LY294002+miR-150组,采用PI3K抑制剂验证LY294002在HT-29细胞凋亡中的作用。结果与空白对照组和NC组相比,miR-150组细胞中miR-150 mRNA水平明显升高(P 0. 05),24 h、48 h、72 h和96h的细胞抑制率明显升高(P 0. 05),细胞凋亡率明显升高(P 0. 05),Bcl-2/Bax、p-PI3K/PI3K和p-Akt/Akt蛋白的表达明显降低(P 0. 05),cleaved Caspase-3蛋白的表达明显升高(P 0. 05);与阴性对照组相比,miR-150组和LY294002组p-Akt/Akt和Bcl-2/Bax蛋白表达均明显降低(P 0. 05),cleaved Caspase-3蛋白表达明显升高(P 0. 05);与miR-150组相比,LY294002+miR-150组p-Akt/Akt和Bcl-2/Bax蛋白表达均明显升高(P 0. 05),cleaved Caspase-3蛋白表达明显降低(P 0. 05)。结论 miR-150过表达可能通过负调控PI3K/AKT信号通路抑制人结直肠癌细胞的增殖,促进其凋亡。     

Genistein对结肠癌细胞HT-29增殖、凋亡的影响及机制探讨

目的观察金雀异黄素(Genistein)对结肠癌细胞HT-29增殖、凋亡的影响,并探讨其作用机制。方法将HT-29细胞分别加入6.25、12.5、25、50、100μg/mL的Genistein进行培养,观察其生长、增殖、凋亡情况并检测其中的Bcl-2、Bax蛋白。结果 25、50μg/mL的Genistein作用48 h后,HT-29细胞的生长受抑制,凋亡率上升(P均<0.01),Bcl-2蛋白表达下降(P均<0.01),Bax蛋白表达上升(P均<0.01),呈剂量依赖性(P<0.05)。各浓度的Genistein作用48 h后对HT-29细胞的增殖有抑制作用,并呈剂量和时间依赖性(P均<0.05)。结论 Genistein既可以抑制HT-29细胞的生长及增殖,又可以诱导其凋亡,其作用机制可能与其上调HT-29细胞Bax蛋白以及下调Bcl-2蛋白的表达有关。     

塞来昔布联合 NK 细胞对裸鼠人肝癌皮下移植瘤生长的影响

目的：观察塞来昔布联合NK细胞对裸鼠人肝癌细胞SMMC-7721皮下移植瘤生长的影响,并探讨其可能的作用机制。方法选择裸鼠40只,制备人肝癌细胞SMMC-7721移植瘤模型,随机分为对照组、NK细胞组、塞来昔布组及联合干预组各10只。 NK细胞组瘤内注射NK细胞悬液0．6 mL,每7 d注射1次,共注射5次;塞来昔布组从接种后第3天起给予塞来昔布100 mg/kg灌胃,每天1次,连续35 d;联合干预组同时给予塞来昔布和NK细胞,给药剂量及途径与单用组相同;对照组灌胃和瘤内注射等量生理盐水。35 d后切取移植瘤组织计算体积,称取瘤质量,并计算抑瘤率;TUNEL法评价肿瘤细胞凋亡情况,免疫组化法检测肿瘤内VEGF、Bax、Bcl-2、caspase-3、Ki-67、NF-κB的阳性表达。结果联合干预组移植瘤体积、肿瘤质量均明显低于单用组（ P均＜0．05）,抑瘤率、凋亡指数明显高于单用组（ P均＜0．05）。联合干预组移植瘤中VEGF、Bcl-2、NF-κB、Ki-67表达明显低于单用组（ P均＜0．05）,Bax、caspase-3表达明显高于单用组（P均＜0．05）。结论塞来昔布联合NK细胞可明显抑制裸鼠人肝癌细胞SMMC-7721皮下移植瘤的生长;其作用机制可能是通过促进凋亡级联通路上Bax、caspase-3的表达,抑制VEGF、Bcl-2、NF-κB、Ki-67的表达而实现。     

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

AIM: To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer (HT-29) cells.METHODS: Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTT assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor y (PPARy), Bcl-2 and Bax in HT-29 cells were analyzed by Western blot.RESULTS: Although rosiglitazone at the concentration below 30 umol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Furthermore, 10 umol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. However, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARy antagonist. Meanwhile, the expression of Bax and PPARy was up-regulated, while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662.CONCLUSION: Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating PPARγ.     

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

AIM:To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer(HT-29)cells.METHODS:Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone.Proliferation and growth of HT-29 cells were evaluated by MTT assay and trypan blue exclusion methods,respectively.The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining.The expressions of peroxisome proliferator-activated receptor γ(PPARγ),Bcl-2 and Bax in HT-29 cells were analyzed by Western blot.RESULTS:Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells,it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition.Furthermore,10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells.However,rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662,a PPARγ antagonist.Meanwhile,the expression of Bax and PPARγ was up-regulated,while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner.However,the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662.CONCLUSION:Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating PPARγ.     

西咪替丁抑制人肠癌裸鼠移植瘤

目的：研究西咪替丁对人结肠癌裸鼠移植瘤生长的抑制作用及机制。方法：建立人结肠癌裸鼠皮下移植瘤模型。随机分2组,每组5只实验鼠。肿瘤种植前3 d开始分别皮下注射生理盐水(对照组)或西咪替丁(治疗组),每天1次,观察成瘤时间及瘤体成长情况。肿瘤种植后第7周处死实验鼠,测定瘤体大小,并用免疫组化方法测定肿瘤组织内微血管密度(MVD)和血管内皮生长因子(VEGF)的表达。结果：治疗组肿瘤体积明显小于对照组;治疗组肿瘤组织中的VEGF表达程度和MVD计数亦明显低于对照组。结论：西咪替丁通过抑制VEGF表达,减少血管生成,从而抑制肿瘤生长。     

腺病毒介导的肿瘤生长抑制因子4和白细胞介素-24双基因共表达对肺腺癌放疗增敏的体内外实验研究

目的 研究肿瘤生长抑制因子4 (ING4)和白细胞介素-24 (IL-24) 双基因共表达腺病毒载体对肺腺癌细胞SPC-A-1的体内外放疗增敏作用及其潜在的作用机制.方法 用Western blot法检测ING4和IL-24在SPC-A-1细胞中的表达;四甲基偶氮唑盐比色(MTT)法和流式细胞仪分别检测Ad-ING4-IL-24联合放疗对SPC-A-1肺腺癌细胞的生长抑制作用和促凋亡作用.应用抽签法将25只裸鼠随机均分为5组:PBS组、腺病毒(Ad)组、双基因组、放疗组及联合组,除放疗组外其余各组均采用瘤体内注射干预用药,隔日1次,共注射6次.第1次治疗前及开始治疗后隔日测量各组瘤体的长径(L)和短径(W),计算瘤体体积(V=L×W2/2),绘制瘤体体积-时间变化曲线.采用 SPC-A-1细胞株建立肺腺癌裸鼠模型,观察Ad-ING4-IL-24联合放疗对移植瘤的抑制作用.免疫组织化学法检测天冬氨酸特异性半胱氨酸蛋白酶-3(Caspase-3)、B细胞淋巴瘤/白血病-2 (Bcl-2)、Bcl-2相关X蛋白(Bax)及血管内皮细胞生长因子(VEGF)基因的表达.采用金正均法计算q值并判断其放疗增敏作用.结果 Western blot法检测结果显示,目的 基因在SPC-A-1细胞中成功表达;MTT和流式细胞仪检测结果显示,Ad-ING4-IL-24联合放疗组对SPC-A-1细胞的生长抑制和促细胞凋亡作用[(86.2±0.8)%、(60.9±1.0)%]明显高于Ad-ING4-IL-24双基因组[(49.8±0.3)%、(26.3±1.3)%]和放疗组[(44.4±2.2)%、(33.3±0.8)%](生长抑制率比较,F=550.88,P＜0.01;凋亡率比较,F=614.08,P＜0.01),Ad-ING4-IL-24联合放疗具有放疗增敏协同作用(q=1.20);裸鼠体内瘤重抑瘤率Ad-ING4-IL-24组、放疗组及Ad-ING4-IL-24联合放疗组分别为49.5%(样本5只)、35.4%(样本5只)和79.8%(样本5只),Ad-ING4-IL-24联合放疗能明显抑制移植瘤生长,具有放疗增敏协同作用(q=1.18);免疫组织化学法检测结果显示,Ad-ING4-IL-24联合放疗可明显上调Bax和Caspase-3基因表达,下调Bcl-2及VEGF基因表达.结论 Ad-ING4-IL-24具有放疗增敏作用,是理想的放疗增敏剂,其作用机制可能与诱导肿瘤细胞凋亡和抑制血管形成有关.

Abstract：

Objective To study the radiosensitivity of the recombinant adenoviral vector (called Ad-ING4-IL-24) carrying and co-expressing inhibitor of growth 4 (ING4) and interleukin-24 (IL-24) to human lung adenocarcinoma and the underlying mechanisms. Methods The expression levels of ING4 and IL-24 were detected by Western blot. The growth-suppressing and apoptosis-inducing effect of Ad-ING4-IL-24 combined with radiotherapy on SPC-A-1 lung carcinoma cells were assessed by MTT assay and FCM respectively. The 25 nude mice were randomly divided into 5 groups of 5 mice ecah: PBS group,Ad group,Ad-ING4-IL-24 group,radiotherapy group and joint group (Ad-ING4-IL-24 combined radiotherapy). Mice in all groups except radiotherapy group were intratumorally injected every other day for 6 cycles. The short and long axes of the tumor were measured dynamically, tumor volume was calculated as: V=L×W2/2, changes in tumor volume were graphed. The human lung carcinoma model was established with SPC-A-1 cells in nude mice. The ratios of tumor-suppression and q were calculated. The expression of Caspase-3, Bcl-2, Bax, VEGF in tumor samples were detected by immunohistochemistry. Results The expressions of ING4 and IL-24 were successfully expressed in SPC-A-1 cells. MTT assay and FCM showed that the levels of cell-growth inhibition and apoptosis induction in Ad-ING4-IL-24 combined with radiotherapy group [(86.2±0.8)%,(60.9±1.0)%] were higher than in Ad-ING4-IL-24 group [(49.8±0.3)%,(26.3±1.3)%] and in radiotherapy group [(44.4±2.2)%,(33.3±0.8)%] (ratio of cell-growth inhibition, F=550.88,P＜0.01; ratio of induced apoptosis F=614.08,P＜0.01). Ad-ING4-IL-24 combined with radiotherapy showed an enhanced radiosensitivity effect on human lung adenocarcinoma(q=1.20). In Ad-ING4-IL-24 group, radiotherapy group and Ad-ING4-IL-24 combined with radiotherapy group, the weight inhibition ratio was 49.5% (5 nude mice), 35.4%(5 nude mice), 79.8%(5 nude mice) respectively. Ad-ING4-IL-24 combined with radiotherapy had a synergetic and enhanced radiosensitivity effect on inhibiting the growth of transplanted tumor(q=1.18). According to immunohistochemistry, Ad-ING4-IL-24 was shown to up-regulate the expression of Bax and Caspase-3 but down-regulate the expression of Bcl-2 and VEGF. Conclusion Ad-ING4-IL-24 had an enhanced radiosensitivity effect on human lung adenocarcinoma, and therefore acted as a radiotherapy sensitizer, which may be related to its effect on apoptosis-induction and antiangiogenesis.     

Effect of Yiqi Jianpi plus anticancer herbs on spleen deficiency in colorectal cancer and its anti-tumor role

Objective:To observe the effect of Yiqi Jianpi plus anticancer herbs on spleen deficiency in colorectal cancer and its anti-tumor role.Methods:Human intestinal cancer cell HT29 xenograft of nude mice model was established.The expression of ECF,VEGF,gastric cancer tumor growth in mice were observed.Results:Protein kinase C expression in in the Yiqi Jianpi group and Yiqi Jianpi anti-tumor group was significantly better than the model group(P0.01,P0.05).There was significantly more apoptotic cells in Yiqi Jianpi anti-tumor group than Yiqi Jianpi group and model group(P0.01).Epidermal growth factor and vascular endothelial growth factor expression in Yiqi Jianpi group was significantly lower than Yiqi Jianpi group and model group(P0.05).Conclusions:Tumor can inhibit the expression of PKC inhibition.Yiqi Jianpi and anticancer treatment can reduce this inhibition.Besides this treatment can also inhibit expression of tumor related genes such as epidermal growth factor and vascular endothelial growth factor.     

Effects of recombinant human growth hormone on growth of human gastric carcinoma xenograft model in nude mice

AIM: To study effects of recombinant human growth hormone (rhGH) on growth of a human gastric carcinoma cell in vivo. METHODS: Experimental mice were divided into control group, rhGH group, oxaliplatin (L-OHP) group and rhGH L-OHP group. Cultured human gastric carcinoma cells BGC823 were inoculated into right axilla of nude mice and carcinoma xenograft model was established successfully. Inhibitory rate of xenograft tumor growth was estimated by measuring tumor volume; expression of proliferating cell nuclear antigen (PCNA), Bax and Bcl-2 proteins of xenograft tumor was detected using immunohistochemical S-P method. RESULTS: Tumor growth inhibitory rate, the positive expression rate of PCNA, Bax and Bcl-2 were 49.3%, 58.2%, 65.2% and 59.2% in rhGH L-OHP group respectively; 46.6%, 62.5%, 59.7% and 64.7% in L-OHP group; 5.0%, 82.7%, 23.2% and 82.2% in rhGH group and 0, 77.8%, 23.5% and 80.3% in control group. There was significant difference between rhGH L-OHP group (or L-OHP group ) and control group or rhGH group (P < 0.05), whereas there were no significant differences (P > 0.05) between L-OHP group and rhGH L-OHP group and between rhGH group and control group. CONCLUSION: rhGH does not accelerate the proliferation of human gastric cancer cell in vivo.