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1.
尿多酸肽对人肝癌细胞Smmu7721体内体外抑制作用   总被引:7,自引:1,他引:6  
目的 :研究由人尿提取的尿多酸肽 (uroacitide)对人肝癌细胞的体内体外抑制作用。方法 :体外实验 ,以四唑盐(MTT)比色法测定培养板中加入尿多酸肽后 ,人肝癌细胞Smmu772 137℃ 5 %CO2 培养箱培养 72h的生物活性 ;体内抑瘤实验为裸鼠皮下接种人肝癌细胞Smmu 772 1,待肿瘤生长后 ,连续每天ip尿多酸肽 10天 ,观察其抑制作用。结果 :体外实验 ,尿多酸肽剂量为 0 0 3~ 2 0 0mg·mL- 1 ,对人肝癌细胞Smmu 772 1的IC5 0 为 0 35~ 0 49mg·mL- 1 ;体内实验 ,尿多酸肽剂量 5 0 0~ 2 0 0 0mg·kg- 1 ,对裸鼠接种人肝癌细胞Smmu 772 1的抑瘤率在 38 9%~ 6 7 9%。结论 :尿多酸肽对人肝癌细胞Smmu772 1体内体外均有显著的抑制作用。  相似文献   

2.
目的研究二肽Lys-Glu(Vilon)的抗肿瘤活性。方法用液相法人工合成了抗肿瘤二肽Vilon,分子量为275.3。用细胞计数法和MTT法测定Vilon对人肠癌LOVO,人胃癌MKN45和人肝癌QGY77033种肿瘤细胞生长的抑制作用,以及对人体正常细胞生长的影响;并对其进行了体内实验。结果Vilon对体外培养的LOVO,MKN45和QGY7703细胞具有剂量依赖性抑制作用,但对人正常白细胞无明显抑制作用。体内抑瘤实验表明,Vilon对小鼠肝癌H22的生长有抑制作用,有效剂量为15mg.kg-1,当使用高剂量30mg.kg-1时,对小鼠移植性肿瘤肝癌H22的抑瘤率达0.60以上,且具有剂效关系。结论Vilon具有明显的体外、体内抗肿瘤活性。  相似文献   

3.
目的评价安体康注射液体外抑瘤作用及对荷瘤小鼠放化疗的增效作用。方法采用结晶紫比色法测定药物对人肺癌G6细胞、人胃腺癌MKN28细胞、人肝癌SMMC7721细胞的抑制作用,用IC50评测其效果。3个剂量给药组(0.45、0.90、1.80 g·kg-1)分别与环磷酰胺、顺氯氨铂、阿霉素合用,2个剂量给药组(0.90、1.80 g·kg-1)分别与60Co照射合用,与单用放化疗药物组比较瘤质量、抑瘤率、增效率。结果安体康注射液对G6、MKN28、SMMC7721细胞的IC50分别为0.381、0.365、0.371 mg·mL-1。合用药各组与相对应的放化疗药物单用组比较,平均瘤质量均小于单用药组,且差异均具有统计学意义(P<0.05)。结论安体康注射液对G6、MKN28、SMMC7721细胞的生长有较强的抑制作用,对荷瘤小鼠环磷酰胺、顺氯氨铂、阿霉素化疗和60Co放疗有增效效应。  相似文献   

4.
目的研究基因重组心肌肌钙蛋白I与人工短肽的融合蛋白(CIS)对肿瘤生长的作用。方法用MTT法观察CIS体外对人脐静脉内皮细胞(HUVEC)生长的作用。利用鸡胚绒毛尿囊膜模型观察CIS对新生血管生长的影响。用6种小鼠肿瘤异位可移植模型观察CIS在体内对肿瘤生长的作用。结果 CIS对HUVEC细胞增殖具有明显抑制作用,并呈剂量依赖关系;鸡胚绒毛尿囊膜实验显示,CIS浓度为5、10 mg·L~(-1)时,新生血管生成的数量明显减少;荷瘤鼠体内异位移植模型实验显示:CIS(10 mg·kg~(-1))处理组肿瘤生长缓慢,瘤体明显小于模型对照组,对S180肿瘤瘤重抑制率85.3%,对Lewis肺癌肿瘤瘤重抑制率87.0%,对H22肝癌肿瘤瘤重抑制率84.2%,对人小细胞肺癌H446肿瘤瘤重抑制率60.42%,对人可移植性肝癌SMMC7721肿瘤瘤重抑制率61.62%,对人胃低分化腺癌BGC823肿瘤瘤重抑制率为41.84%。结论 CIS在体外抑制HUVEC细胞的生长,在鸡胚绒毛尿囊膜实验中,CIS对新生血管生成有明显的抑制作用。在体内,CIS融合蛋白可有效抑制小鼠可移植肿瘤细胞的生长。CIS抗肿瘤效应很可能是通过抑制肿瘤组织中血管内皮细胞的增殖,进而减少肿瘤组织中新生血管生成的数量而达到的。  相似文献   

5.
聚酯型儿茶素对人肝癌细胞生长的抑制作用及其机制   总被引:3,自引:1,他引:2  
目的 探讨聚酯型儿茶素对人肝癌SMMC 772 1细胞的生长抑制作用及其机制。方法 应用MTT法、集落形成试验、同位素掺入试验、细胞内cAMP/cGMP浓度测定、原位杂交等方法进行检测。结果  5 0mg·L-1聚酯型儿茶素对SMMC 772 1细胞的生长、集落形成有明显的抑制作用 ;[3H] TdR、[3H] Leu掺入试验证明其可明显抑制细胞DNA和蛋白质合成 ;聚酯型儿茶素作用后 ,SMMC 772 1细胞内cAMP及cGMP浓度明显增加 ,细胞的c myc基因mR NA水平表达明显降低 ,而 p5 3基因mRNA水平表达明显升高。结论 聚酯型儿茶素对肝癌SMMC 772 1细胞的生长有明显的抑制作用 ,此作用与其抑制细胞DNA和蛋白质合成、升高细胞内cAMP浓度和抑制c myc基因表达、增强p5 3基因表达有关  相似文献   

6.
目的探讨胡桃楸提取物SH体内外抗肿瘤活性。方法体外实验应用MTT法检测SH对人宫颈癌细胞株HeLa、小鼠腹水型肝癌细胞株Hca-F的增殖抑制作用;体内实验应用小鼠S180实体瘤动物模型,通过对荷瘤小鼠体质量以及抑瘤率的影响,评价SH不同剂量(4.5、9.0、18.0 mg·kg-1)以及与化疗药物环磷酰胺(cyclophosphamide,CTX)联合用药对S180肉瘤的生长抑制作用。结果体外实验表明,SH可以显著抑制HeLa、Hca-F肿瘤细胞的增殖;体内实验表明,SH具有明显的抑瘤作用,中、高剂量组(9、18 mg·kg-1)的抑瘤率分别为25.9%和35.3%,与CTX联合用药时,能够提高CTX的抑瘤率,中、高剂量组(9+10 mg·kg-1、18+10 mg·kg-1)抑瘤作用呈现相加作用。结论胡桃楸提取物SH,在体外能够明显抑制HeLa、Hca-F肿瘤细胞的增殖,在体内能够抑制荷瘤小鼠S180肉瘤生长,提示胡桃楸提取物SH具有一定的抗肿瘤活性。  相似文献   

7.
目的 :研究骆驼蓬硷对小鼠移植性肿瘤体内及体外肿瘤细胞的抗癌试验。方法 :体内抑瘤实验采用S -1 80 ,肝癌H2 2 及艾氏腹水癌等荷瘤小鼠、体外实验采用Hela细胞和S -1 80细胞。结果 :骆驼蓬硷对小鼠移植性肿瘤的抑制率在 2 8 94 % -4 6 77%之间 ,对肿瘤细胞的平均生长抑制率在 83 4 1 % -92 30 %之间。结论 :骆驼蓬硷对肿瘤细胞体内抑瘤试验、体外细胞毒试验均有明显的抑制作用。  相似文献   

8.
目的:研究鸡血藤提取物的体内与体外抗肿瘤作用。方法:采用mT法检测鸡血藤提取物对体外培养的5种肿瘤细胞增殖的抑制作用;体内试验采用小鼠实体瘤S180细胞株接种小鼠,建立实体瘤与腹水瘤模型。计算抑瘤率与生命延长率。结果:鸡血藤提取物在5μg/ml-80μg/ml剂量的范围内对5种肿瘤细胞均有抑制作用。体内试验小鼠分另吐灌胃给予20mg/kg、50mg/kg、100mg/kg,能抑制小鼠体内肿瘤增长。也能明显提高腹水瘤小鼠的生命延长率。结论:鸡血藤提取物在体外对不同组织来源的肿瘤细胞增殖有明显的抑制作用;在体内能抑制小鼠体内瘤体生长,明显延长小鼠的生存期。  相似文献   

9.
纳米雄黄抗肿瘤作用及在荷瘤小鼠组织中的分布   总被引:4,自引:3,他引:4  
目的:研究纳米雄黄抗肿瘤作用和在荷瘤小鼠体内的分布情况,并与原料雄黄进行比较。方法:采用计算抑瘤率的方法研究纳米雄黄对动物移植瘤生长的影响,应用MTT法检测纳米雄黄对体外培养人肿瘤细胞株生长的抑制作用,用石墨炉原子吸收光谱法检测荷瘤小鼠组织样品砷浓度。结果:纳米雄黄对小鼠艾氏腹水癌实体型和小鼠肝癌H22均有抑制作用,且纳米雄黄50 mg·kg-1剂量组的抑瘤作用与原料雄黄100mg·kg-1剂量组的抑瘤作用相当。纳米雄黄对HL-60细胞和U937细胞的抑制作用强于原料雄黄。纳米雄黄组肝、脾、肿瘤中砷浓度显著高于同剂量原料雄黄组。结论:纳米雄黄抗肿瘤作用强于原料雄黄,并具有肝、脾和肿瘤组织靶向性。  相似文献   

10.
目的探讨一种灵芝提取物体内外抗肿瘤作用。方法应用小鼠H22肝癌移植瘤模型,研究灵芝提取物的体内抗肿瘤作用;采用MTT法检测灵芝提取物的体外抗肿瘤活性。结果①灵芝提取物对H22移植瘤呈剂量依赖性抑制作用,500 mg.kg-1组的瘤重抑制百分率达59.3%,与阴性对照组比较有统计学差异(P〈0.01);②MTT法检测显示灵芝提取物对K562和HL60两种瘤株有较强抑制作用,对SMMC7221、HepG2、SW480、SW1116和SGC7901五种瘤株抑制作用较弱。结论灵芝提取物在体外及体内均有较强的抗肿瘤作用,其有效成分及机制有待进一步研究。  相似文献   

11.
Antitumor activity of spergualin, a novel antitumor antibiotic   总被引:2,自引:0,他引:2  
Spergualin (SGL), a novel antitumor antibiotic, exhibited strong antitumor activity against transplantable leukemias in mice: L1210, L1210(IMC), P388, P815, C1498, EL-4 and RL male 1. It also exhibited antitumor activity against M5076 fibrosarcoma, AH66 and AH66F rat hepatomas, but not against Meth-A fibrosarcoma, B16 melanoma, Lewis lung carcinoma (LL) and C26 colon adenocarcinoma. The antitumor activity of SGL was administration-schedule dependent. The strongest activity against L1210 was obtained by ip continuous infusion for 7 days or daily ip administration for 9 days. Single ip injection of SGL at 100 mg/kg to mice caused convulsion and death within 15 minutes after injection. Such acute toxicity was not observed by continuous infusion. SGL showed its strongest activity at subtoxic dose against sensitive tumors except for L1210(IMC). Mice implanted ip with L1210(IMC) were cured by treatment with SGL at 3.13 mg/kg/day for 9 days, but died from the tumor at 50 mg/kg/day X 9. The cured mice rejected a second inoculation of up to 10(6) tumor cells. The tumor cells isolated from mice after treatment with the high dose showed resistance to SGL in vivo. Mice implanted sc with L1210(IMC) were also cured by 9 daily ip administrations of SGL at 12.5 mg/kg/day, but solid tumor was observed at the implantation site until 3 days after the final injection of SGL in some cured mice. These results suggest that the therapeutic effect of SGL has a relatively high specificity for leukemias and that the immunological effect is involved in the antitumor activity.  相似文献   

12.
To study the antitumor activity of alkaloid extracted from Oxytropis ochrocephala and its possible mechanism, we observed the effect of alkaloid on tumor weight and expression of PCNA and p53 in mice bearing H(22) hepatocellular carcinoma by means of immunohistochemistry SP method. After treatment with alkaloid from Oxytropis ochrocephala, the results showed that alkaloid administration (25 and 50 mg/kg body weight, p.o.) could inhibit H(22) hepatocellular carcinoma growth to various extent, and the rates of inhibition were 48.5% and 57.7% respectively (p<0.01). The antitumor activity of the alkaloid is in a dose dependent manner, with no signs of toxicity to weight, kidney and liver. The sections of tumor showed the number of tumor cell decreased and nucleus appeared putrescence such as nucleus atrophy, disintegrating and dissolving. Meanwhile, the expression of PCNA and mutant p53 protein positive cell numbers in mice bearing H(22) hepatocellular carcinoma also suppressed by alkaloid (p<0.05). It suggested that Alkaloid from Oxytropis ochrocephala showed antitumor effect and its possible mechanism might be associated with the expression inhibition of PCNA and mutant p53 protein. Further studies are needed to explore the antitumor activity of the other compounds of Oxytropis ochrocephala and to specify their possible mechanism of action.  相似文献   

13.
Mangosteen (Garcinia mangostana) has been widely used in the traditional medicine of Thailand to treat various ailments, especially diseases of the digestive system and infections. Many reports show antiproliferation of crude extracts and active constituents from mangosteen against many cancer cell lines. Therefore, the current study is proposed to demonstrate in vivo evidence on the antitumor activity of mangosteen. Crude methanolic extract (CME) from mangosteen pericarp including 25.19 % α-mangostin as an active xanthone was used in this study. The inhibition on tumor cell proliferation of CME was preliminarily evaluated against the murine colon cancer cell line NL-17 with an IC50 value of 17 and 84 μg/ml based on WST-1 and LDH assays, respectively. The safety dose for animal application was assessed by in vivo toxicity studies using female BALB/c mice. Acute toxicity showed an LD50 value and approximate lethal dose at 1,000 mg/kg, whereas the suitable dose for short-term study should be ≤200 mg/kg. The effective dose for antitumor activity of CME was found to be between 100 and 200 mg/kg, with a tumor size reduction of 50–70 %. Histological staining clearly illustrated a decrease of tumor cell density in the footpad in a dose-dependent manner. The median survival time and life span significantly increased in tumor-bearing mice with CME treatment. This study suggests that CME possesses a powerful antitumor activity. Therefore, it is worth undertaking further investigation to identify active compounds and obtain a deeper understanding of their mechanism, in order to acquire novel effective anticancer drugs.  相似文献   

14.
多肽ND100的抗肿瘤活性研究   总被引:5,自引:2,他引:5  
目的 研究多肽ND100的抗肿瘤活性。方法 用液相法人工合成了抗肿瘤八肽ND100,分子量为 846 9。测定了ND100对 3种小鼠移植性肿瘤的抑制作用,并研究了ND100对小鼠红细胞和白细胞数量的影响。结果 体内抑瘤试验表明,ND100对小鼠H22肝癌、小鼠Lewis肺癌和小鼠S180肉瘤的生长均有明显抑制作用,有效剂量为 2 5mg·kg-1,当使用高剂量时(15mg·kg-1 )时,对 3种小鼠移植性肿瘤的抑制率达 0 70以上,且具有剂效关系。ND100对小鼠红细胞和白细胞的数量均无影响。结论 ND100具有明显的体内抗肿瘤活性。  相似文献   

15.
The novel alkylating dipeptide melphalanyl-p-L-fluorophenylalanine ethyl ester (J1) was evaluated for acute toxicity and antitumor activity in mice, with melphalan as a reference. To determine a safe and tolerable dose for efficacy studies the acute toxicity following intravenous injection in the tail vein was monitored using a 14-day schedule with up to four doses. The highest tested dose, 25 micromoles/kg, was considered close to this level, with minor effects on body weight gain but significant effects on hematological parameters. Melphalan and J1 appeared equitoxic with no statistically significant differences. Subsequently a mouse hollow fiber model was employed with subcutaneous implantation of fibers containing human tumor cells. Three different human tumor cell lines as well as two samples of primary human tumor cells (ovarian carcinoma and chronic lymphatic leukemia) were used as tumor models. At the dose level tested there was a marked and statistically significant decrease in both T-cell leukemia CCRF-CEM and small cell lung cancer NCI-H69 tumor cell growth and viability in response to J1 as compared with both placebo and melphalan treated groups. In primary ovarian carcinoma cells only J1 treatment resulted in significant tumor regression (net cell kill). In summary the results indicate that, despite an expected short half time in the blood circulation, the promising in vitro data from the previous studies of J1 seems translatable into the in vivo situation. At equal doses of alkylating units J1, compared to melphalan, was more active in the mouse hollow-fiber model, but showed similar general toxicity.  相似文献   

16.
目的对合成的一系列凡德他尼衍生物进行体内外抗肿瘤活性的筛选,为寻找低毒高效的新型酪氨酸激酶抑制剂研究提供依据。方法体外筛选采用均相时间分辨荧光(HTRF)法和磺酰罗丹明B(SRB)法分别进行激酶和细胞的筛选;采用经典的急性毒性实验方法,并建立移植人非小细胞肺癌H1975裸鼠模型评价其抗肿瘤活性。结果 HTRF结果显示有6个活性较好的化合物(TY8115、TY8119、TY8122、TY8128、TY8129、TY8131),其中TY8115对VEGFR-2和EGFR抑制作用均好于凡德他尼;SRB结果显示这些活性化合物对选用的3种靶细胞(A431、H1975、A549)均有不同程度的抑制作用,其中TY8115的肿瘤细胞增殖抑制作用最明显,且对非靶细胞(MDA-MB-231)生长影响很小;急性毒性实验结果显示TY8115没有表现出毒性反应;体内抗肿瘤活性研究结果显示TY8115对肺癌H1975具有疗效,75、150 mg/kg TY8115对H1975的相对肿瘤增殖率分别为54.44%、39.54%。结论化合物TY8115具有良好的抗肿瘤活性,并且毒副作用小,具有发展成为一种新型酪氨酸激酶抑制剂的潜力。  相似文献   

17.
The antitumor effect of a polyamine biosynthetic pathway inhibitor methylglyloxal bis(butylamidinohydrazone) (MGBB) on human malignant melanoma (HMG) cells and its combination effect with cisplatin were investigated. The growth of cultured HMG cells was inhibited in a dose dependent manner by either MGBB or cisplatin; complete inhibition of cell proliferation was attained with 5 micrograms/ml of MGBB or 50 micrograms/ml of cisplatin. Pretreatment of HMG cells with MGBB diminished the antitumor action of cisplatin. The cultured HMG cells were inoculated in nude mice and aliquots of the resulting solid tumors (HMG tumor) were transplanted. The growth of transplanted HMG tumors in mice was inhibited markedly by cisplatin (3.8 mg/kg) and moderately by MGBB (10 or 20 mg/kg). The in vivo antitumor effect of cisplatin was also reduced by combined treatment with MGBB.  相似文献   

18.
Cyclophosphamide (CTX) is in the nitrogen mustard group of alkylating antineoplastic chemotherapeutic agents. It is one of the most frequently used antitumor agents for the treatment of a broad spectrum of human cancers. Thioredoxin reductase (TrxR) catalyze the NADPH-dependent reduction of thioredoxin and play an important role in multiple cellular events related to carcinogenesis including cell proliferation, apoptosis, and cell signaling. This enzyme represents a promising target for the development of cytostatic agents. The purpose of this study is to determine whether CTX could target TrxR in vivo. Lewis lung carcinoma and solid H22 hepatoma treated with 50-250 mg/kg CTX for 3 h lost TrxR activity in a dose-dependent fashion. Over 75% and 95% of TrxR activity was lost at the dose of 250 mg/kg. There was, however, a recovery of TrxR activity such that it attained normal levels by 120 h after a dose of 250 mg/kg. In addition, we found that CTX caused a preferential TrxR inhibition over other antioxidant enzymes, such as glutathione peroxidase, catalase, and superoxide dismutase. We also used ascites H22 cells to investigate cancer cells response after TrxR was inhibited by CTX in vivo since CTX is needed to be activated by liver cytochrome P450 enzymes. The time course and dose-dependent changes of cellular TrxR activity were similar with those in tumor tissue. CTX caused a dose-dependent cellular proliferation inhibition which was positively correlated with TrxR inhibition at 3 h. Furthermore, when 3 h CTX-treated cells with various TrxR backgrounds, harvested from ascites-bearing mice, were implanted into mice, the proliferations of these cells were again proportionally dependent on TrxR activity. The TrxR inhibition could thereby be considered as a crucial mechanism contributing to anticancer effect seen upon clinical use of CTX.  相似文献   

19.
蚯蚓纤溶酶的抗肿瘤作用   总被引:9,自引:0,他引:9  
目的 观察蚯蚓纤溶酶 (EFE)对体外人癌细胞株及体内人癌裸鼠移植性肿瘤生长的影响 ,对该药进行临床前抗肿瘤药效学评价。方法 采用MTT法观察蚯蚓纤溶酶对体外人癌细胞的生长抑制作用 ;用人胃癌BGC82 3和人乳腺癌B37裸鼠移植性肿瘤模型对蚯蚓纤溶酶进行体内抗肿瘤药效学观察。结果 蚯蚓纤溶酶在体外对人癌细胞的生长无抑制作用 ;灌胃给予蚯蚓纤溶酶 2 0 0~ 10 0 0mg·kg-1,可明显抑制人胃癌BGC82 3和人乳腺癌B37裸鼠移植性肿瘤的生长。结论 蚯蚓纤溶酶具有抗肿瘤作用。  相似文献   

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