重组人白细胞介素-6抑制BTT739小鼠膀胱癌生长和转移的实验研究

目的　探讨重组人白细胞介素 6对小鼠膀胱癌BTT739生长和转移的抑制作用。方法将BTT739肿瘤细胞接种于T739近交系小鼠皮下 ( 2 6× 10 5/小鼠 ) ,2 4只小鼠随机分成 3组 ,第 3天始分别给予对照组溶剂 ( 0 9NS) 0 3mL ,治疗组重组人白细胞介素 6( 4× 10 6IU kg) ,日 2次 ,腹腔注射 ,共 2 0天 ,阳性对照组MMC ( 1mg kg)日 1次 ,腹腔注射计 14天。第 2 5天测对照组和治疗组的皮下瘤重及肺转移率 ,分别进行t检验和 χ2 检验。结果　两组皮下瘤重分别为 11 4± 1 9g和 7 4± 0 8g ,重组人白细胞介素 6有明显抑制BTT739肿瘤生长作用 ,抑瘤率 35 1% (P<0 0 5) ,而对肺转移灶数目及转移灶大小的抑制率分别为 61 3%和 2 6 2 % (P值均 <0 0 5) ,有显著性差异。结论　重组人白细胞介素 6可明显抑制BTT739小鼠膀胱癌生长和转移。     

重组人白细胞介素-6治疗小鼠膀胱癌机制的实验研究

目的 :探讨重组人白细胞介素 - 6 (rhIL 6 )对BTT739荷瘤小鼠的抗肿瘤作用机制。方法 :BTT739肿瘤细胞接种T739小鼠 ,随机分组 :1)对照组 :腹腔注射生理盐水 0 2mL ,每日 1次 ;2 )rhIL 6组 :每日腹腔注射 1次rhIL 6 ,剂量为 4× 10 6IU/kg小鼠体重 ;应用电镜、流式细胞分析技术检测细胞凋亡 ;用流式细胞仪检测肿瘤细胞膜Fas与FasL受体及Bcl 2蛋白的表达。结果 :rhIL 6组小鼠肿瘤组织电镜下可见特征性凋亡细胞的出现 ,流式细胞仪检测出在G1期前出现凋亡峰较对照组明显增加 ,P <0 0 5 ;Fas与FasL的表达较对照组明显增加 ,rhIL 6组升至 12 5 7%和 2 0 1% ,而对照组仅为 4 6 6 %和 14 1% ,经检验P <0 0 5 ;Bcl 2蛋白的表达较对照组无明显变化 ,经检验P >0 0 5。结论 :rhIL 6可以诱导小鼠膀胱癌细胞凋亡 ,死亡受体Fas及FasL的表达增加 ,可能是rhIL 6诱导肿瘤细胞凋亡的重要信息传导途径     

依维莫司负调控mTOR信号通路对膀胱癌BTT739细胞增殖和迁移的抑制作用及机制研究

目的:探索mTOR抑制剂依维莫司(RAD001)对膀胱癌BTT739细胞在体外和小鼠体内增殖和迁移的抑制作用及其作用机制,为依维莫司在临床上治疗膀胱癌提供理论依据。方法:体外培养小鼠膀胱癌BTT739细胞,待其生长至对数期后用梯度浓度的RAD001（0 nmol/L、5 nmol/L、10 nmol/L和20 nmol/L）干预24 h,用MTT法检测细胞增殖的变化;Tranwell实验检测RAD001对BTT739细胞迁移的影响;ELISA试剂盒检测细胞分泌蛋白E-钙黏蛋白表达的变化。Western blot检测Akt、mTOR、4EBP和PTEN蛋白的表达,RT-PCR检测mTOR mRNA的表达。将BTT739细胞接种于昆明鼠皮下,待成瘤后,用依维莫司干预14天,取小鼠肿瘤组织检测E-钙黏蛋白及AKT、mTOR、4EBP和PTEN蛋白表达的情况。结果:体外实验显示RAD001可以抑制BTT739细胞的增殖和迁移并与剂量有关（P＜0.05）。还可以增加E-钙黏蛋白的含量,抑制癌细胞的转移。实验证明RAD001在体外抑制Akt、mTOR、4EBP的表达,促进肿瘤抑制因子PTEN的表达（P＜0.05）。将BTT739细胞接种于小鼠皮下后发现,RAD001在小鼠体内亦可以抑制病变情况,促进PTEN和E-钙黏蛋白的表达,抑制Akt、mTOR和4EBP的表达。结论:mTOR抑制剂依维莫司通过抑制mTOR信号通路抑制膀胱癌细胞BTT739的增殖、迁移和侵袭。     

紫杉醇对Lewis肺癌抑制作用及机理的研究

目的　探讨紫杉醇对Lewis肺癌生长和转移的抑制作用。方法　将Lewis肺癌细胞接种于C5 7BL/6小鼠皮下 ,腹腔注射紫杉醇 1 0mg/kg ,连续 1 0d。处理动物后测量治疗组及对照组皮下瘤重、肺转移灶计数 ,应用流式细胞术测定肿瘤细胞凋亡率 ,并进行光镜和电镜观察。结果　对照组和治疗组皮下瘤重分别为 (2 .833± 0 .0 74)g和 (0 .5 88± 0 .0 40 )g(P <0 .0 1 ) ,肺转移灶计数分别为 (5 .5 0 0± 0 .92 6 )个和(1 .1 6 7± 0 .75 3)个 (P <0 .0 1 ) ,肿瘤细胞凋亡率分别为 9.0 0 2 %和 2 5 .772 % (P <0 .0 1 )。电镜观察紫杉醇组可见典型的凋亡细胞和凋亡小体。结论　紫杉醇可明显抑制小鼠Lewis肺癌的生长和转移 ,并可诱导肿瘤细胞凋亡     

四君子汤通过Fas受体诱导小鼠膀胱癌细胞凋亡

目的:探讨中药四君子汤对小鼠膀胱癌BTT739的抗肿瘤作用机制。方法:小鼠膀胱癌细胞接种于T739小鼠皮下,动物抽签法随机分为三组,对照组:生理盐水每次0·15mL,每日2次灌胃;四君子汤小剂量组:四君子汤每次0·15g,每日1次灌胃;四君子汤大剂量组:四君子汤每次0·3g,每日2次灌胃。每组小鼠接种24h后分别给药;用药14d后应用电镜、流式细胞分析技术检测各组小鼠膀胱癌细胞凋亡,流式细胞仪检测肿瘤细胞膜Fas与FasL受体的表达。结果:电镜下可见四君子汤大剂量组小鼠肿瘤组织特征性凋亡细胞的出现,而其他组未出现上述征象;流式细胞仪检测四君子汤大剂量组肿瘤细胞的凋亡峰值为(20·11±1·32)%,四君子汤小剂量组及对照组为(9·33±1·62)%和(5·91±1·84)%,经比较差异有统计学意义,P=0·0001;四君子汤大剂量组肿瘤细胞Fas与FasL的表达为(12·47±0·51)%和(21·3±0·49)%,较其他两组明显增加,P=0·0002。结论:在本实验条件下,大剂量组四君子汤可以诱导小鼠膀胱癌细胞凋亡,死亡受体Fas及FasL的表达增加,可能是四君子汤诱导肿瘤细胞凋亡的重要信息传导途径。     

放射和高聚生对小鼠膀胱癌生长的抑制作用

 目的　研究放射和高聚生 (HASL)对小鼠膀胱癌生长的抑制作用。方法　将BTT739肿瘤细胞接种于T739小鼠皮下制成模型 ,观察不同放射剂量及高聚生对局部肿瘤的抑制作用。结果　接种后即给予HASL治疗 ,第 16dHASL组、放射 5Gy组、放射 5Gy加HASL组的抑瘤率依次为 34%、5 3.2 %、5 2 .9%。接种后 7d给予HASL治疗 ,抑瘤率依次为 2 7.0 %、5 4.9%、6 4.6 % ,放射 8Gy组、放射 8Gy加HASL组依次为 80 .7%、84 .1%。结论　HASL对局部肿瘤生长有抑制作用 ,但与放射联合时不增加放射对肿瘤的抑制作用。     

血管生成抑制剂TNP-470抑制肝癌生长和转移的实验研究

目的　研究血管生成抑制剂TNP 470对肝细胞癌生长和转移的抑制作用。方法　把高转移人肝癌模型(LCI D2 0 )的肿瘤组织小块种植于裸鼠皮下 ,将 2 4只裸鼠随机分成对照组、治疗组。第 2天起分别给予溶剂 ( 3%酒精 )、TNP 470 ( 30mg kg)隔天皮下注射 ,共 8次。 结果　对照组、治疗组皮下瘤重分别为 ( 2 0 4± 0 34)g、( 0 98± 0 34) g(P<0 0 0 1) ;两组AFP分别为 ( 76 8 6± 2 82 3) μg L ,( 93 4±5 8 6 ) μg L (P <0 0 0 1) ,两组肺转移率分为5 0 % ( 6 12 )、8 3 % ( 1 12 ) (P <0 0 5 )。结论　血管生成抑制剂TNP 470能显著抑制肝细胞癌的生长和转移     

尿胰蛋白酶抑制剂Ulinastatin 对lewis 肺癌小鼠肿瘤生长和转移的抑制作用

 目的　探讨尿胰蛋白酶抑制剂(U TI) 在动物模型上抗肿瘤作用。方法　选用尿胰蛋白酶抑制剂乌司他丁(Ulinastatin) , Lewis 肺癌小鼠模型;雄性C57BL/ 6 小鼠40 只,接种lewis 肿瘤细胞,分成生理盐水组(对照组) 、环磷酰胺组(CTX) 、Ulinastatin 2. 5万单位组、Ulinastatin 5 万单位组、Ulinastatin 10万单位组,各8 只,接种后第6 天,开始腹腔给药,记录皮下瘤长短径变化,做生长曲线;接种14 天后处死所有小鼠,统计皮下平均瘤重和肺转移灶个数, 使用流式细胞计分析凋亡率(AR) 增值百分比(SPF) 。结果　皮下瘤重依次为(7. 92 ±2. 52 、0. 66 ±0. 50^＊＊ 、3. 47 ±1. 45^＊ 、3. 08 ±0. 81^＊＊、1. 70 ±1. 05^＊＊) g ,平均肺转移灶依次为( 8. 625 ±1. 407 、1. 125 ±1. 126^＊＊、1. 625 ±1. 302^＊＊ 、1. 00 ±0. 75^＊＊ 、0. 625 ±0. 74^＊＊) 。CTX 组(39. 3 ±4. 8) %^＊ 和Ulinastatin 10 万单位组(40. 2 ±3. 1) %^＊的AR 值明显增加,Ulinastatin 未见SPF 值明显减少。结论　Ulinastatin 对lewis 肺癌小鼠的转移瘤生长和自发性肺转移有抑制作用。     

联合自杀基因与IL-2基因转移疗法的抗肿瘤效果及其抗肿瘤免疫应答的诱导作用

单用自杀基因疗法或单用细胞因子基因疗法抗肿瘤效果不理想,本研究中我们观察了大肠杆菌胞嘧啶脱胺酶(CD)基因与白细胞介素2(IL-2)基因联合转移对荷瘤小鼠的治疗效果及其对抗肿瘤免疫的诱导作用。复制荷瘤小鼠模型后在荷瘤部位注射表达CD基因的重组腺病毒(AdCD)及表达小鼠IL-2基因的重组腺病毒(AdIL2),并连续10天、每天1次腹腔注射5氟胞嘧啶(5FC)对荷瘤小鼠进行治疗。结果表明,AdCD/5FC/AdIL2联合基因治疗能显著抑制荷瘤小鼠皮下肿瘤的生长,并明显延长其生存期(P<0.01)。联合基因治疗组小鼠肿瘤细胞发生明显的坏死,瘤内及瘤周有大量的炎性细胞浸润,瘤内CD4~ 和CD8~ T细胞明显增加,脾细胞NK和CIL杀伤活性明显高于单用AdCD/5FC、对照病毒AdLacZ/5FC或PBS组。实验结果表明,联合应用自杀基因与细胞因子基因治疗可更有效诱导机体的抗肿瘤免疫反应,从而更显著地抑制荷瘤小鼠肿瘤的生长。     

生长激素对荷瘤小鼠化疗效果影响的实验研究

目的 :探讨外源性生长激素对荷瘤小鼠化疗效果的影响。方法 :将 6 0只 6 15小鼠随机分为两群 ,一群用于观察肿瘤生长情况 (36只 ) ,一群用于观察生存期 (2 4只 )。每群动物经脾脏接种小鼠前胃癌细胞 (MFC)建立肝转移模型后 ,再随机分为 3组 :对照组、化疗组和联合组。术后 2周对照组每天皮下及腹腔注射生理盐水 ;化疗组每天腹腔注射 5 FU 2 0mg/kg ;联合组每天皮下注射重组人生长激素 (rhGH) 2IU/kg ,腹腔注射 5 FU 2 0mg/kg。各组均连续用药 7天。 4周时处死第一群动物 ,第二群小鼠待其自然死亡或观察满 70天处死。结果 :化疗组和联合组的肝转移瘤数目较少 ,肝重量和肝脏指数明显较低 (P <0 0 5 ) ,生存期也明显延长 (P <0 0 5 )。肿瘤细胞周期分析显示 ,联合组静止期 (G0 /G1)细胞百分比高于其它两组 (P<0 0 5 ) ,S期细胞百分比和增殖指数 (PI)均低于其它两组 (P <0 0 5 )。结论 :rhGH与 5 Fu合用抑制了肿瘤生长 ,可延长动物生存期 ,而对化疗效果无不良影响 ;rhGH可能通过加速细胞增殖周期 ,提高周期特异性化疗药物的敏感性     

Antitumor effects of recombinant human Interleukin-6 on mouse bladder carcinoma through Fas-mediated apoptosis

Purpose

An apoptosis-inducing therapy is gradually becoming a new strategy for cancer treatment. The aim of this study was to investigate the mechanism of growth-inhibitory effects of recombinant human interleukin-6 (rhIL-6) on bladder tumor-bearing T739 mice in vivo.

Methods

Murine bladder transitional carcinoma cells (BTT739) were inoculated subcutaneously into T739 mice as a tumor model for evaluating the antitumor effects of rhIL-6. Then the mice were divided randomly into 5 groups: A, B, C, D and E. Different doses (0, 2, 4, 8 × 10⁶ IU/kg body weight) of rhIL-6 were injected intraperitoneally twice per day and administered for 14 days, and 1 mg/kg/d mitomycin-C(MMC) was used as control. Tumor size was measured and determined as the mean of the largest diameter and the diameter at right angle. Animals were killed by CO₂ inhalation on the 15th day after tumor cell inoculation. Then, tumors were removed, weighed and collected. The tumor growth inhibition rate of rhIL-6 was calculated. The morphological characteristic changes of tumor cells were observed under electron microscope, and cell cycle analysis was determined by flow cytometry. The expressions of Fas, FasL and Bcl-2 protein on tumor cells were qualitatively detected by immunofluorescence cell staining, and their relative contents (rate of positive cells, RPC) were quantitatively determined with flow cytometry.

Results

rhIL-6 could inhibit bladder tumor growth in a dose-dependent manner in vivo. The tumor growth-inhibitory rates of 2, 4, 8 × 10⁶ IU/kg rhIL-6 and 1 mg/kg MMC were 11.8, 39.5, 39.7 and 68.8%, respectively. Flow cytometry results showed that a hypodiploid peak before G1 phase could be found in tumor cells treated with rhIL-6. Moreover, the cells treated with rhIL-6 displayed disappearance of nucleoli, chromatin gathering under the nuclear membrane in mass or ring-shape under transmission electron microscopy. The rates of Fas, FasL protein–positive cells estimated by flow cytometry in rhIL-6-treated mice were (12.57 ± 0.83) and (20.1 ± 0.87) %, respectively, significantly higher than that (4.66 ± 0.17) and (14.1 ± 0.83) % in control mice (P < 0.01). There was no significant difference in the rate of Bcl-2 protein–positive cells between the mice in these two groups (P > 0.05).

Conclusions

rhIL-6 had obvious antitumor effects on mouse bladder carcinoma in vivo, and the Fas signaling pathway might play an important role in rhIL-6-induced bladder carcinoma cell apoptosis.     

小鼠可移植性膀胱移行细胞癌株（BTT739）的建立及实验研究

用化学致癌剂ＢＢＮ诱异Ｔ７３９近交系小鼠膀胱肿瘤，于诱癌２６周时，将其中１只雄性小鼠膀胱癌往同种系小鼠皮下移植获成功。於１９９１年５月２５日建立了我国第一株小鼠可移植性膀胱癌模型，经２年多时间，已移植传代５６代次，其生物学和病理学特征已相对稳定，在同系小鼠移植成功率１００％，无自然消退现象，带瘤小鼠平均存活５４天，病理组织学检查证实ＢＴＴ７３９为低分化小鼠膀胱移行细胞癌，经２０种抗癌药物药敏试验结果表明对其中的１６种显示不同程度敏感。     

Potentiation of chemotherapeutic activity by a Chinese herb medicine juzen-taiho-toh

Antitumor activity of Juzen-Taiho-Toh (JTX) and combination effect of JTX with antitumor agents were studied using murine tumors. In order to determine the antitumor activity of JTX, mice inoculated ip with IMC carcinoma (1 X 10(6) cells/CDF1 mouse), sarcoma-180(1 X 10(6) cells/ICR mouse) or Meth-A fibrosarcoma (1 X 10(6) cells/BALB/c mouse) were treated with JTX (12.5-50 mg/kg/day) ip on day 1 through day 10, and the survival days of mice were examined. Treatment with 25 mg/kg/day produced 38.7% increase of life span against IMC carcinoma. However, no antitumor effect was observed on solid form of these tumors by the daily treatment with JTX. Combination effect of JTX and antitumor agents was also examined. ICR mice inoculated sc with 1 X 10(6) cells of sarcoma-180 on day 0 were treated with JTX (2,000 mg/kg/day) po on day-7 through day 30. In addition, some of these groups received mitomycin C (5 mg/kg), cytoxan (67 mg/kg) or adriamycin (2.5 mg/kg) iv on days 3, 8 and 11, and the size of tumor grown in sc site was measured by a caliper. In combination with JTX, mitomycin C resulted in a significantly greater tumor growth inhibition than could be obtained with mitomycin C alone. Secondly, BALB/c or C57BL/6 mice inoculated sc with 1 X 10(4) cells of Meth-A fibrosarcoma or 1 X 10(5) cells of B16 melanoma on day 0 were treated with JTX (2,000 mg/kg/day) po on day 1 through day 30. Some of these group received ip with mitomycin C (3 mg/kg), adriamycin (2 mg/kg), 5-FU (33 mg/kg) or cytoxan (67 mg/kg) on days 3, 6, 9, 12, 15 and 18. From this result, the group treated with JTX and mitomycin C also showed a higher tumor-growth inhibition. Thus, a combination of a high dose of mitomycin C with JTX was more effective than mitomycin C alone.     

快速大容量尾静脉注射法构建循环肝癌细胞肝转移小鼠模型

目的： 通过快速大容量尾静脉注射方法构建循环肝癌细胞肝内复发转移小鼠模型。 方法： 40只C57BL/6J小鼠采用随机数字表法随机分为对照组和实验组（20只/组）,对照组采用传统的缓慢小容量尾静脉注射法（2×10 6个肝癌Hepa1-6细胞/0.2 ml,30 s内注射完毕）,实验组采用改良的快速大容量尾静脉注射法（2×10 6个肝癌Hepa1-6细胞/2 ml,5 s内注射完毕）构建循环肝癌细胞肝内复发转移小鼠模型。4周后摘取肝、肺、肾、脾组织并行H-E染色,大体和镜下观察肝脏、肺脏、脾脏和肾脏的成瘤情况。 结果： 对照组小鼠只在肺脏有转移灶形成,成瘤率为95%（19/20）,肝脏、肾脏、脾脏未见有转移灶形成。实验组小鼠在肝脏和肺脏同时形成转移灶,肺脏成瘤率为94.7%（18/19）,肝脏成瘤率为100%（19/19）,脾脏、肾脏未见转移灶形成。 结论： 快速大容量尾静脉注射法注射循环肝癌细胞构建的小鼠模型可以模拟肝癌根治性切除后残留的循环肝癌细胞导致早期肝癌肝内复发转移的过程。     

A novel immunocompetent murine tumor model for the evaluation of RCAd-enhanced RDAd transduction efficacy

Low gene transfer rate in tumors, high dose-induced acute inflammatory response, and lack of an immunocompetent preclinical animal model to accurately reflect the therapeutic efficacy are prominent reasons for the lack of clinical success of adenoviral (Ad) vectors. In this study, we tested whether human replication-competent adenovirus (RCAd) can replicate in T739 mouse bladder transitional tumor cells (BTT) and lung adenocarcinoma cells (LA795), and whether RCAd can enhance the transduction rate and transgene expression of human replication defective adenoviruses (RDAd) in these tumor cells in vitro and in vivo. We demonstrated that human RCAd exhibited good infectability and cytopathologic effects in mouse BTT and LA795 cells, which was comparable to that in A549 and NCIH460 human tumor cells. In contrast, no infectability and cytopathologic effects were observed in other three mouse tumor cells such as 4T1, B16, and Lewis cells. The combined use of RCAd with RDAd significantly enhanced RDAd transduction efficiency in BTT and LA795 tumor cells in vitro and in vivo. When BTT and LA795 cells were co-infected with RDAd Ad-EGFP and RCAd, a large amount of E1a expression and 2-3 orders of increases in Ad-EGFP genomic DNA were observed. In contrast, the expression of the late gene Hexon is very low, which may explain ineffective packaging of viral particles. In conclusion, our study provided a novel immunocompetent animal model which is useful for evaluating RCAd infectability, cytopathy, and replication. The combined use of RCAd and RDAd provided a new solution for cancer gene therapy.     

坎地沙坦对子宫内膜癌血管生成的影响

目的：探讨血管紧张素Ⅱ-1型受体（Angiotensin Ⅱ type 1 receptor,AT1R）拮抗剂坎地沙坦是否通过抑制肿瘤血管生成而抑制子宫内膜腺癌裸鼠荷瘤模型肿瘤生长.方法：将24只BALB/C裸鼠随机分成3组,建立子宫内膜癌裸鼠荷瘤模型,分为对照组、坎地沙坦10mg·kg-1·d-1组,坎地沙坦100mg·kg-1·d-1组.观察各组裸鼠成瘤时间、测量肿瘤体积、绘制成瘤曲线并计算抑瘤率.免疫组化法检测皮下移植瘤血管内皮生长因子（vascular endothelial growth factor,VEGF）和微血管密度（microvascular density,MVD）的不同.结果：与对照组相比,两组坎地沙坦组皮下移植瘤体积均显著减少（P＜0.05）,并且两组坎地沙坦组皮下移植瘤VEGF、MVD的表达明显降低（P＜0.05）.结论：AT1R拮抗剂坎地沙坦可以抑制肿瘤的血管生成,从而抑制子宫内膜癌的生长,故AT1R拮抗剂将可能成为治疗子宫内膜癌的一种新型药物.     

联合应用Ag85A和GM-CSF DNA疫苗对小鼠移植性膀胱癌BTT739细胞瘤免疫治疗的研究

目的:探讨联合应用Ag85A与GM-CSF DNA疫苗对小鼠移植性膀胱癌BTT739细胞瘤免疫治疗的效果。方法:选用小鼠膀胱癌BTT739细胞株,构建T739小鼠移植瘤模型。随机数字表法分为5组:生理盐水组、空载体组、Ag85A组、联合应用组和BCG组。荷瘤后第7天、14天和21天各肌注1次,末次注射后第7天检测各组小鼠脾脏的CD4+和CD8+T细胞亚群数量及CD4+/CD8+比值、血清IFN-γ和肿瘤重量。结果:与生理盐水组对比,单独应用Ag85A和联合应用Ag85A与GM-CSF DNA疫苗均能够升高CD4+和CD8+T细胞的百分比及CD4+/CD8+的比值,提高血清IFN-γ浓度,降低移植瘤重量,差异具有统计学意义(P<0.05)。联合应用的效果要明显优于单独应用组,差异具有统计学意义(P<0.05),但尚不及单纯应用BCG的免疫治疗效果。结论:联合应用Ag85A与GM-CSF DNA疫苗能够提高荷瘤小鼠的免疫功能,从而达到了抑制肿瘤生长的作用,其效果明显优于单独应用Ag85A DNA疫苗,二者联用具有协同增强免疫效应。     

全反式维甲酸对人膀胱癌细胞株T24生长 抑制和凋亡诱导作用的实验研究

 目的　探讨全反式维甲酸(ATRA)对人膀胱癌细胞T24的生长抑制和凋亡诱导作用。方法　应用细胞和分子生物学技术检测不同浓度ATRA对T24细胞生长和凋亡的影响。结果　3×10-5M～3×10-7M ATRA可显著抑制T24细胞增殖。用3×10-5M和3×10-6M ATRA作用细胞6天出现典型凋亡特征;3×10-5M、3×10-6M组及对照组的细胞凋亡率分别为20.16%、15.31%和1.49%;DNA琼脂糖凝胶电泳呈现凋亡特征性的DNA梯形带。结论　ATRA对人膀胱癌细胞T24有剂量生长抑制作用,且可成功地诱导人膀胱癌细胞T24发生凋亡。