硒化亚油酸的抗癌作用研究

用作者首次合成的硒化亚油酸进行体内外抗癌活性实验,结果表明,硒化亚油酸对小鼠EAC移植瘤有较强的抑制作用;体外对S_(180)腹水型癌细胞有明显的直接杀伤作用。     

金环蛇毒心脏毒对S180,EAC腹水癌细胞的细胞毒性作用

目的：探讨金环蛇毒心脏毒对S180,EAC腹水癌细胞的细胞毒性作用。方法：采用小白鼠腹腔和皮下接种S180,EAC腹水癌细胞造成小白鼠腹水模型后腹腔注射金环蛇毒心脏毒。结果：腹腔注射金环蛇毒心脏毒,能抑制肿瘤细胞的生长,降低接种率。但不能完全控制腹水和癌细胞的生长。体外试验表明有明显的细胞毒作用。台酚蓝染色镜检可见死细胞显著增加,腹水图片检查,给药后细胞膜破裂,纤维化坏死明显。结论：能延长小白鼠存活时间。     

东亚钳蝎毒抗癌多肽抗肿瘤作用的体内试验

目的：研究东亚钳蝎毒抗癌多肽（anticer polypeptide from Buthus Martensii Venom,APBMV）的细胞毒作用和体内抗癌作用。方法：体外试验用噻唑蓝还原法（MTT法）检测APBMV对体外培养的人结肠癌细胞（Lovo,HT-29）、人胃癌细胞（SGC－7901）的生长抑制作用。建立小鼠移植瘤模型，观察APBMV腹腔注射以及口腔给药对S－180肉瘤的体内抑瘤作用。结果：体外试验表明，APBMV对Lovo、SGC－7901和HT－29细胞的半数抑制浓度（IC50）依次为60、71、139μg/ml。体内试验表明，APBMV9、6、3mg/kg，腹腔注射作用10d后，对小鼠S－180肉瘤的平均抑瘤率依次为64％、53％和47％，与对照组相比有统计学意义。结论：APBMV对多种人消化道肿瘤细胞有较强的生长抑制作用，并对小鼠移植癌具有抑制作用。     

毛萼乙素纳米混悬剂.Ⅱ.对小鼠肝癌H22移植瘤的生长抑制作用

采用小鼠肝癌H22移植性肿瘤模型,考察不同给药途径和剂量下,毛萼乙素纳米混悬剂的抗肿瘤作用及毒性.在适宜的给药剂量下,毛萼乙素纳米混悬剂经静脉注射、腹腔注射和灌胃3种途径给药均可抑制小鼠肝癌H22移植瘤的生长,并呈现明确的量效关系,但其毒性也随着剂量的增加而明显增大.在10 mg/kg的剂量下,腹腔注射的抑瘤作用优于静脉注射;但该途径给药产生的毒性也比静脉注射大.灌胃给药的抑瘤作用最弱,且高剂量时会产生严重的胃肠道不良反应.     

马氏珠母贝全脏器提取物糖胺聚糖抗肿瘤作用的实验研究

目的 :观察马氏珠母贝 (pinctadamartensis )全肉提取物糖胺聚糖精提物 (glycosaminoglycan ,GAG)或粗提物 (coarseglycosaminoglycan ,CGAG)对几种肿瘤的作用。方法 :用昆明种小鼠 ,分别观察GAG和CGAG对体内几种肿瘤的抑瘤率、生命延长率、与 5 FU或替加氟的协同作用 ,及其对体外培养HL 6 0细胞的杀伤作用。结果 :糖胺聚糖粗、精提取物分别对体内S180肉瘤和艾氏腹水癌 (EAC)有显著增敏 5 FU或替加氟的抑瘤作用 ,抑瘤率分别达 6 1.96 %或4 6 .30 % ;糖胺聚糖精提物对S180肉瘤生命延长率影响明显 ,生命延长率为 14 .16 % ;糖胺聚糖粗提物(1.0g·L- 1或 0 .1g·L- 1)对体外培养HL 6 0细胞杀伤率达 38.6 7%或 2 5 .6 4%。结论 :糖胺聚糖粗、精提物分别对体内S180肉瘤和EAC有显著增敏 5 FU或替加氟的抑瘤作用 ,并有一定的提高生命延长率的作用 ,对体外培养HL 6 0细胞还有一定的杀伤作用     

抗癌胶囊对实验性肿瘤的治疗及对化疗减毒作用研究

目的：研究抗癌胶囊对小鼠移植肿瘤S180，H22，Lewis的抑瘤作用及对化疗药所致小鼠免疫功能抑制的保护作用。方法：按照抗癌药物筛选规程进行体内抑瘤实验：采用氟尿嘧啶（FU）制备免疫功能低下模型，测定抗癌胶囊对小鼠白细胞计数、免疫器官重量、腹腔巨噬细胞吞噬功能和NK细胞的影响。结果：抗癌胶囊对小鼠移植肿瘤S180，H22，Lewis均有不同的抑瘤作用，其中高剂量组抑瘤效果最佳，并对小鼠体重生长无明显影响。抗癌胶囊还有明显拮抗FU所致白细胞下降，胸腺、脾脏萎缩，腹腔巨噬细胞功能降低和NK细胞减少等毒副作用。结论：抗癌胶囊具有明显的抗肿瘤作用。     

2种给药方式的胂酸基乙酸对H_(22)肝癌荷瘤小鼠的抑瘤作用比较

目的 :比较不同给药方式的胂酸基乙酸 (ASAC)对H22 肝癌移植瘤在小鼠体内生长的抑制作用。方法 :采用腹腔注射和静脉注射2种给药方式 ,分别在小鼠右腋皮下接种肝癌H22 细胞后 ,随机将其分为5组 ,分别注射生理盐水、环磷酰胺及不同剂量的ASAC ,观察癌细胞株的成瘤率、受试物对H22 肝癌荷瘤小鼠的抑瘤作用及其对小鼠脏器的影响。结果 :与腹腔注射给药方式比较 ,静脉注射给予ASAC高、中、低剂量后均产生显著抑制肿瘤生长作用 ,其抑瘤率分别为46. 59 %、46 .31 %和32 .48 % ;2种给药方式的ASAC低剂量组小鼠脾重指数均有升高 ,但静脉注射给予ASAC高剂量组出现了小鼠中毒死亡。结论 :与腹腔注射给药方式比较 ,ASAC静脉注射给药方式的抑瘤作用更好。     

中药抑瘤胶囊体内抗肿瘤作用研究

目的：观察中药抑瘤胶囊体内抗肿瘤作用。方法：体内抑瘤试验采用4种小鼠移植性肿瘤细胞（S－180，Hep-A-22,U14和EAC）腋部皮下接种，次日开始连续给药10天，每天给药1次，给药途径为灌有（ig)，然后杀鼠取瘤称重，比较各组肿瘤生长抑制率。结果：中药抑瘤胶囊对S－180，Hep-A-22,U14小鼠移植肿瘤生长抑制率为35－60％之间，与对照组比较P＜0．05。结论：中药抑瘤胶囊对S810，Hep-A-22,U14等小鼠移植肿瘤生长具有明显的抑制作用。     

灵芝孢子多糖抗移植性肿瘤实验研究

目的研究灵芝孢子多糖的抗癌作用。方法采用小鼠抗移植性肿瘤实验方法。结果灵芝孢子多糖分别以150 mg.kg-13、00 mg.kg-1和600 mg.kg-1剂量连续12天灌胃给药,对小鼠移植性肝癌Heps的抑瘤率为53.77%~65.25%;连续8天灌胃给药,对小鼠移植性肉瘤S180的抑瘤率为50.39%~55.04%,皆呈良好的抑瘤作用。灵芝孢子多糖可分别提高Heps和S180荷瘤小鼠的脾指数和胸腺指数。结论灵芝孢子多糖有良好的抑瘤作用,并可增强Heps和S180荷瘤小鼠的非特异性免疫功能。     

中药提取物RX体内抗肿瘤作用研究

目的观察中药提取物RX体内抗肿瘤作用。方法体内抑瘤试验采用4种小鼠移植性肿瘤细胞（S-180、Hep-A-22、U14和EAC）腋部皮下接种，次日开始连续给药10d，每天给药1次，给药途径为灌胃（ig），然后将鼠处死取瘤称重，比较各组肿瘤生长抑制率。结果中药提取物RX对S-180、Hep-A-22、U14小鼠移植肿瘤生长抑制率为35％～60％之间，与对照组比较P〈0．05。结论中药提取物RX对S180、Hep-A-22、U14等小鼠移植肿瘤生长具有明显的抑制作用。     

重组L—门冬酰胺酶与其野生型在体外和体内的抗肿瘤作用比较

目的:研究重组L-门冬酰胺酶对肿瘤细胞体外生长及实验性肿瘤的抑制作用.方法:体外培养肿瘤细胞(K562、L1210和P815),分别用倒置显微镜和透射电镜观察肿瘤细胞的形态学,MTT比色法观察细胞增殖率及抑制率,流式细胞仪分析DNA含量.同时根据移植性肿瘤研究方法小鼠接种L1210、P388、Heps及S_(180)瘤株,观察给药后小鼠存活天数和瘤重.结果:体外细胞培养实验证明,重组L-门冬酰胺酶对K562、L1210和P815细胞生长具有显著抑制作用(P<0.01).体内实验表明,重组L-门冬酰胺酶ip能显著延长移植肿瘤小鼠(L1210和P388)的存活天数(P<0.01),并对小鼠移植性肝癌实体瘤(Heps)生长有明显的抑制作用(P<0.01)。重组L-门冬酰胺酶iv对小鼠Heps和S_(180)肿瘤生长有明显的抑制作用(P<0.01).结论:重组L-门冬酰胺酶对肿瘤细胞体外生长及受试肿瘤有明显抑制作用.本结果对重组L-门冬酰胺酶的临床应用提供实验依据.     

金丝马尾连碱甲等成分的抗肿瘤作用

从金丝马尾连提取的总生物碱及其主要成分碱甲(hernandezine)对P388白血病小鼠、腹水型S180及C26结肠癌小鼠有一定的治疗作用。在体外,碱甲明显地抑制小鼠白血病L1210细胞及人口腔癌KB细胞的生长,对小鼠正常造血祖细胞(CFU-GM)的抑制作用较弱。初步结果表明,碱甲可阻断G₁细胞向S期过渡,其杀细胞作用似为细胞周期特异性。金丝马尾连的其它两个成分碱乙(thalidezine)及碱丙(isothalidezine)也有类似的抑制癌细胞作用。     

一些植物成分对实验肿瘤的作用

观察了18个植物成分对S180、Lewis肺癌、B16黑色素瘤、Ehrlich腹水癌、白血病P388、L1210和L615等小鼠肿瘤的疗效。以白血病P388和L1210最为敏感,L615最不敏感。此外,试验了高三尖杉酯碱、美登素、羟基喜树碱和长春新碱对Friend白血病的疗效,仅高三尖杉醋碱有明显疗效。部分样品还观察了对~3H标记的前体参入肿瘤细胞核酸和蛋白质的影响。     

Antitumor effect of kazusamycin B on experimental tumors

Kazusamycin B, a novel antibiotic (MW 542) isolated from fermentation broth of Streptomyces sp. No. 81-484 showed a broad antitumor spectrum both in vitro and in vivo. IC50 against the growth of tumor cells was around 1 ng/ml at 72 hours-exposure in vitro. Intraperitoneal injection of the antibiotic was effective in inhibiting the growth of murine tumors, S180, P388, EL-4, and B16. It was also active against doxorubicin-resistant P388, hepatic metastases of L5178Y-ML, pulmonary metastases of 3LL, and human mammary cancer MX-1 xenografted to nude mice. However, the activity of kazusamycin B toward L1210 or human lung cancer LX-1 was weaker. According to the results of comparative studies on the effect of kazusamycins B and A, an analog of B, there seemed to be no significant difference in their effectiveness. The effective dose range and toxicity were markedly dependent on tumor lines tested and the regimen used. Maximum tolerated dose in mice with subcutaneous tumors was much higher than that in mice bearing ascitic leukemia as P388. Although intermittent administration could greatly reduce the cumulative toxicity of the drug, therapeutic effect was similar with both successive and intermittent administration schedules.     

千金子Ⅰ号体内外抗肿瘤药理作用的实验研究

目的　观察千金子Ⅰ号体内、外抗肿瘤活性及对免疫器官的影响。方法　体外药效试验用MTT法 ,观察千金子Ⅰ号对人宫颈癌细胞 (HeLa)增殖作用的影响 ;体内用小鼠移植性肿瘤 ,采用荷瘤小鼠瘤重、抑瘤率检测千金子Ⅰ号对肉瘤 180 (S180 )和艾氏腹水癌 (EAC)的抑制作用 ;通过检测胸腺指数、脾脏指数等指标观察千金子Ⅰ号对免疫器官的影响。结果　千金子Ⅰ号体外对HeLa细胞的增殖有显著的抑制作用 ;对荷瘤小鼠肉瘤 180 (S180 )和艾氏腹水癌 (EAC)也有抗肿瘤活性。结论　千金子Ⅰ号具有一定的体内外抗肿瘤活性 ,同时对免疫功能又无影响     

In vivo antitumor activity of 4-amino 4-methyl 2-pentyne 1-al, an inhibitor of aldehyde dehydrogenase

4-amino-4-methyl-2-pentyne-1-al (AMPAL), a new irreversible inhibitor of aldehyde dehydrogenase (ALDH) has been assayed for its in vitro and in vivo antitumor activity. In vitro, AMPAL inhibits the proliferation and the ALDH activity of L1210 and RBL5 cell lines. In vivo, AMPAL significantly increases the mean survival time of mice i.p. grafted with leukemia (L1210, P815, MBL2, EL4, RBL5 cell lines) or carcinoma cells (Krebs cell line), without haematopoetic toxicity. No carcinostatic effect was observed against the P388 leukemia and the 3LL Lewis lung carcinoma. A possible relationship between the ALDH isoenzyme activity of the tumor and its sensitivity to AMPAL is discussed in the light of previous reports concerning the role of aldehydes in cell growth control.     

Modulation of thiol pools by vitamin K3 and its effect on survival of sensitive and resistant murine tumor cells.

Cytotoxic effects of vitamin K3 were evaluated utilizing the P388/S, L1210, EAT, S-180 and a multidrug-resistant variant of the P388 leukemia cells (P388/ADR). Antitumorigenic potential of vitamin K3 was assessed by MTT and DNA and RNA biosynthesis inhibition assay. A dose-dependent inhibition of P388/S and P388/ADR cell survival and [3H]thymidine and [3H]uridine incorporation (as a function of DNA and RNA biosynthesis) was observed in tumor cell types exposed to vitamin K3 concentrations ranging from 1 to 100 microM. One hundred mg/kg vitamin K3 caused a 32 and 52% increase in life span of the sensitive and resistant P388 leukemia tumor-bearing mice. Induction of DNA strand breaks at 100 microM vitamin K3 was greater in P388/S than in P388/ADR cells. In vitro treatment with vitamin K3 (100 microM) reduced the intracellular levels of GSH by 40, 47, 6, 15 and 14% in P388/S, P388/ADR, EAT, S-180 and L1210 tumor cells, respectively. In vivo treatment with 100 mg/kg vitamin K3 reduced the GSH content by 18 and 38% and increased the activity of the enzyme GSH-S-transferase and gamma-glutamyl transpeptidase. Effects of free radical scavengers and of compounds that modulate the GSH metabolism on the cytotoxicity of vitamin K3 were also investigated. Results indicate that vitamin K3 interacts with the tumor cell thiol pools while eliciting its antitumor effects and suggest the utility of vitamin K3 in dealing with the growing problem of multidrug resistance.     

海南粗榧新碱衍生物HH07A的抗肿瘤作用

用细胞生长曲线测定法及软琼脂集落形成分析法研究了HH07A对几种肿瘤及正常细胞生长的影响。结果表明,1.5ug·ml^-1及3μg·ml^-1HH07A能分别明显抑制L1210和HL-60细胞的生长。3种肿瘤细胞对HH07A的敏感性依次为L1210>KB>HL-60,而正常小鼠粒系祖细胞GM-CPC对药物的敏感性则低于前三者,且HH07A3.5μg·ml^-1对HL-60细胞无分化诱导作用。HH07A对腹水型L1210白血病小鼠、S180小鼠均有较明显的治疗作用,使L1210荷瘤小鼠、S180荷瘤小鼠存活时间延长。也能抑制S180实体瘤的生长。     

1,2∶5,6-二去水卫矛醇与美登新联合用药的实验研究

去水卫矛醇(DAG)和美登新(MAY)同时或间隔24小时给药(无论先后顺序如何),对EAC小鼠的生命延长和杀瘤细胞均有协同作用;不同先后顺序给药对L1210得到同样结果,但同时给药则无协同作用。给DAG后24小时再给MAY,对接种21天的B16黑色素瘤瘤重抑制率超过了“相加作用”,但不能延长生命。联合用药对HepA及S180无协同疗效。联合使用DAG及MAY,对正常小鼠骨髓干细胞的杀灭低千“相加作用”。本实验表明,DAG及MAY间隔24小时给药较同时给药为佳。     

Antitumor effects of royal jelly (RJ)

Antitumor effects of Royal Jelly (RJ) were investigated employing the transplantable tumors of mouse advance leukemia L1210 and P388 strains and Ehrlich, Sarcoma-180 ascites and solid tumor strains. RJ was administered orally in a prophylactic-therapeutic (30 days before and 30 days after the transplantations of tumor cells) or a therapeutic (30 days after the transplantations of tumor cells) manner. Tumor cells were transplanted i.p. (ascites tumor) or s.c. (solid tumor). The daily dose of RJ was 0 (control), 10, 100, or 1000 mg/kg. In the case of the therapeutic experiments employing advance leukemia L1210 and P388 strains, which gave quite a short survival period of 8 approximately 9 days, RJ did not show any antitumor effect. In the case of the therapeutic RJ application employing the Sarcoma-180 ascites tumor, which gave a moderate survival period of 16 days, the increased life span was 9.3 approximately 19.3%; and with the Ehrlich ascites tumor (survival period of 22.1 days), the increased life span was 20.4% (RJ 10 mg/kg . day) and 17.6% (RJ 1,000 mg/kg . day), but no antitumor effect was observed at the dose of 100 mg/kg . day. In the case of the therapeutic experiment employing Ehrlich solid tumor, tumor growth inhibition was 25.3 approximately 54.8%, where as the use of the prophylactic-therapeutic regimen gave a tumor growth inhibition of 38.3 approximately 45.7%. In the case of the therapeutic RJ application employing Sarcoma-180 solid tumor, tumor growth inhibition was 45.1 approximately 59.7%, where as the prophylactic-therapeutic regimen gave a tumor growth inhibition of 49.1 approximately 56.1%.(ABSTRACT TRUNCATED AT 250 WORDS)