水溶性壳聚糖对肝癌细胞生长抑制的实验研究

目的 观察壳聚糖对肝癌细胞SMMC7721的生长抑制作用.方法 采用MTT法研究了不同浓度水溶性壳聚糖对肝癌细胞株SMMC7721的生长抑制作用.结果 水溶性壳聚糖可抑制肝癌细胞的生长,在一定范围内(50～400mg/L)呈剂量依赖关系.结论 水溶性壳聚糖对肝癌细胞的生长有抑制,并且呈剂量依赖关系.     

壳聚糖及其衍生物对肝癌细胞SMMC7721的生长抑制作用

目的观察壳聚糖及其衍生物对肝癌细胞SMMC7721的生长抑制作用。方法采用四甲基偶氮唑盐(MTT)法研究了不同浓度水溶性壳聚糖、磺化壳聚糖、羧甲基壳聚糖和壳寡糖对肝癌细胞株SMMC7721的生长抑制作用。结果在4种不同壳聚糖及其衍生物中,水溶性壳聚糖和磺化壳聚糖可显著抑制肝癌细胞的生长,并在一定范围内(50~400 mg/L)呈剂量依赖关系,其中以磺化壳聚糖最为显著,羧甲基壳聚糖和壳寡糖对肝癌细胞无生长抑制作用。结论壳聚糖及其衍生物可抑制肝癌细胞的生长,并且呈剂量依赖关系。     

青蒿对鼻咽癌细胞CNE-1、SUNE-1生长的影响

目的研究青蒿对鼻咽癌细胞系CNE-1、SUNE-1的生长抑制作用。方法①采用血清药理学的方法提取中草药青蒿的含药血清;②采用MTT法检测青蒿对CNE-1、SUNE-1细胞生长的抑制作用。结果 MTT法证实青蒿含药血清对鼻咽癌细胞CNE-1、SUNE-1细胞生长均有抑制作用;在SUNE-1细胞中无剂量-效应关系和时间效应关系;在CNE-1细胞中有剂量-效应依赖关系,无时间-效应依赖关系;结论青蒿含药血清对SUNE-1、CNE-1细胞的生长有抑制作用。     

PPAR-γ的激动剂吡咯列酮抑制肝癌细胞生长的实验研究

目的观察PPAR-1的激动剂吡咯列酮对肝癌细胞的生长抑制作用。方法采用MTT法研究了不同浓度盐酸吡咯列酮与肝癌细胞株SMMC7721的生长抑制作用,并观察了不同时间对SMMC7721的生长抑制作用。结果吡咯列酮对肝癌细胞有明显抑制作用,随着浓度的升高吡咯列酮对肝癌细胞的生长抑制作用逐渐增强;在高浓度组（20μM以上）,在一定的时间范围内（24—120h）随着作用时间延长,抑制作用逐渐增强。结论PPAR-1的激动剂吡咯列酮可抑制肝癌细胞的生长,并且呈剂量和时间依赖关系。     

多西紫杉醇对人胆囊癌细胞的体外抑制作用

目的初步探索多西紫杉醇对人胆囊癌细胞的体外抑制作用。方法用不同浓度(1、2、4、8、16、32、64μg/mL)的多西紫杉醇处理人胆囊癌GBC-SD细胞24、48、72h,采用MTT方法检测多西紫杉醇对GBC-SD细胞增殖的影响。结果多西紫杉醇对胆囊癌细胞有明显的生长抑制作用,并且在一定范围内存在着剂量依赖关系和时间依赖关系。结论多西紫杉醇能够有效抑制胆囊癌细胞的生长。在对胆囊癌的化疗过程中,多西紫杉醇有着巨大的潜力。     

红甜菜提取物对HeLa细胞增殖和荷瘤鼠瘤体生长的影响

目的研究红甜菜提取物对人宫颈癌HeLa细胞增殖和对荷瘤小鼠肿瘤生长的抑制作用。方法采用细胞计数法观察红甜菜提取物对HeLa细胞的抑制作用,在人宫颈癌荷瘤鼠模型上观察红甜菜提取物对肿瘤生长的抑制作用,并用病理切片观察瘤体细胞变化。结果甜菜提取物对人宫颈癌HeLa细胞具有抑制作用,并具有剂量-时间依赖关系。荷瘤鼠动物实验表明,红甜菜提取物对裸鼠肿瘤生长也具有抑制作用,剂量为20mg/d时抑瘤率为40%;摄入红甜菜提取物组的裸鼠瘤体细胞出现坏死。结论红甜菜提取物对HeLa细胞的生长和对荷瘤裸鼠肿瘤生长具有抑制作用。     

广西五步蛇毒小肽的分离纯化及抗肿瘤作用

目的：从广西五步蛇毒分离出小分子活性组分，研究其对肿瘤细胞株的抑制作用。方法：经Sephadex G-75凝胶过滤、超滤和DEAE—Sepharose—CL-6B离子交换层析法从广西五步蛇毒中分离纯化获得一种小分子的肽类，采用MTT法检测其对多种体外培养的癌细胞株的生长抑制情况。结果：从广西五步蛇毒中分离纯化得到的单一的小肽，其对卵巢癌细胞株（A2780）、人胃癌细胞（SGC-7901）以及鼠乳腺癌细胞株（782）有抑制作用并呈明显的剂量依赖关系，作用24h的IC50分别为0．264、0．648、0．173μg／mL。结论：应用凝胶过滤和离子交换层析方法可以从广西五步蛇毒中分离出单一组分的小分子肽，其对多种肿瘤细胞的生长有抑制作用。     

钩藤碱对豚鼠结肠带收缩反应的影响

以维拉帕米为对照,观察了钩藤碱对豚鼠离体结肠带收缩反应的影响。钩藤碱对乙酰胆碱或高钾去极化后Ca~(2+)诱发的结肠带收缩均产生剂量依赖性抑制作用,量效曲线显示,钩藤碱呈非竞争性拮抗CaCl_2作用,pD’_2值为4.94±0.05。在无钙液中钩藤碱与维拉帕米相似,能抑制乙酰胆碱诱发的结肠带收缩,表明对结肠带依赖细胞内Ca~(2+)的收缩有抑制作用。当恢复细胞外液Ca~(2+)浓度后,维拉帕米对依赖细胞外Ca~(2+)所致收缩无明显影响,而较大剂量的钩藤碱却产生明显抑制作用。     

皖南尖吻蝮蛇蛇毒中抗肿瘤活性蛋白分离纯化及其活体外性研究

目的:分离纯化皖南尖吻蝮蛇蛇毒(Wannan Agkistrodon acutus venom)中抗肿瘤活性蛋白并研究其活性。方法:利用DEAE-sepharose Fast Flow和SP-sepharose Fast Flow阴阳离子交换层析以及Sephadex G-75凝胶过滤层析等分离方法从皖南尖吻蝮蛇蛇毒中分离纯化得一种抗肿瘤活性蛋白,用CCK-8法检测该蛋白对体外培养的白血病K562细胞、结肠癌细胞(SW480)、胃癌细胞(SGC7901)、肝癌细胞(HepG2)的增殖抑制作用。结果:分离纯化得一相对分子质量约23700的抗肿瘤活性组分(ATF1-c),CCK-8检测对体外培养的K562、SW480、SGC7901、HepG2细胞的增殖抑制作用,呈剂量-时间依赖关系。结论:ATF1-c对体外培养的人癌细胞有明显的抑制和杀伤作用。     

精氨酸剂量与肿瘤生长的相关性研究

探讨了不同剂量的精氨酸与肿瘤生长的相关性 ,进而阐明了精氨酸对肿瘤生长影响的剂量依赖关系。结果提示 ,平衡氨基酸能促进肿瘤生长 ,一定剂量的增量精氨酸对肿瘤生长有抑制作用 ,而超大剂量的精氨酸则促进肿瘤生长     

CCK-8法检测AT#9对肿瘤细胞的生长抑制作用

目的:研究复方制剂AT#9 的体外抗肿瘤作用.方法:采用细胞毒性检测CCK-8 法检测AT#9 对小鼠乳腺癌细胞EMT6、人肺癌细胞A549 和人前列腺癌细胞PC3M 的体外抑制生长作用.结果:AT#9 对三种肿瘤细胞的半数抑制浓度IC50 分别为1824μg/ml、3219μg/ml 和5854μg/ml.结论:AT#9 在体外对三种不同的肿瘤细胞有不同程度的生长抑制作用,且呈浓度依赖关系.     

Biological activities of Portuguese propolis: Protection against free radical-induced erythrocyte damage and inhibition of human renal cancer cell growth in vitro

This study reports for the first time the biological properties of Portuguese propolis. The antioxidant potential of propolis samples from Bornes (Northeast) and Fundão (Centre) regions of Portugal was evaluated by their ability to inhibit the 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidative hemolysis and lipid peroxidation in human erythrocytes. Bornes and Fundão propolis strongly protected the erythrocyte membrane from hemolysis (IC₅₀ of 6.3 ± 0.7 and 10.4 ± 2.7 μg/ml, respectively), in a time- and concentration-dependent manner. This effect was found to be significantly higher than that presented by ascorbic acid (IC₅₀ of 31.0 ± 5.6 μg/ml). In addition, human erythrocytes treated with propolis extracts showed concentration-dependent decrease in levels of malondialdehyde, a breakdown product of lipid peroxidation. Propolis extracts were also assayed for their anticancer properties on human renal cell carcinoma (RCC). Primary cultures of normal and cancerous renal cells derived from RCC patients, in addition to A-498 cell line, were treated with propolis extracts (0-100 μg/ml). Cytotoxic and antiproliferative effects were determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Propolis extracts exhibited selective toxicity against malignant cells compared to normal cells. In vitro RCC growth was strongly inhibited by Bornes and Fundão propolis in a concentration-dependent manner. Our results indicate that Portuguese propolis constitutes an excellent source of effective natural antioxidant and chemopreventive agents.     

茵陈素对肺癌细胞增殖和细胞周期的影响

目的 :探讨茵陈素对肺癌细胞增殖和细胞周期的影响。方法 :应用光镜、四氮甲唑蓝 (MTT)方法和流式细胞术分析茵陈素对肺癌细胞形态学、生长和细胞周期的变化。结果 :茵陈素能抑制肺癌细胞的增殖 ,呈剂量依赖性 ,以160μg/ml抑制作用最明显 ,抑制率达52 4 %。80μg/ml时 ,S期和G2/M期细胞比例开始下降 ,细胞被阻滞于G0/G1 期 ,不能进入S期及G2/M期 ,增殖指数明显下降。结论 :茵陈素在体外对肺癌细胞具有抑制作用 ,通过抑制DNA合成 ,将细胞阻滞于G0/G1 期来抑制细胞增殖。     

黄芪皂苷对人胃癌细胞系MKN-74 增殖与侵袭的影响

目的探讨黄芪属植物黄芪的根部的一种提取物——黄芪皂苷(astragaloside,AST)在体外对胃癌MKN-74细胞增殖与侵袭力的影响。方法用五个不同剂量(0,2.5,5,10,20μmoL.L-1)的和胃癌MKN-74细胞共培养24、48、72小时,通过MTT法检测黄芪皂苷(AST)对细胞的抑制作用;Transwell侵袭实验检测黄芪皂苷对MKN-74细胞侵袭力的抑制作用。结果 (1)AST在体外能够显著抑制胃癌MKN-74细胞的增殖,2.5μmoL.L-1,5μmoL.L-1,10μmoL.L-1,20μmoL.L-1黄芪皂苷处理72小时生长抑制率分别为4.65%,7.58%,20.73%,30.38%,呈现明显的剂量和时间依赖性。(2)AST显著抑制MKN-74细胞的侵袭力,呈现剂量和时间依赖性。结论 AST在体外对人胃癌MKN-74细胞有显著的抑制细胞增殖作用。     

兖州卷柏活性物质提取及对人食管癌细胞的抑制作用

摘要目的研究兖州卷柏水提的工艺优化,并检测兖州卷柏水提物的总抗氧化水平和对人食管癌细胞株Ec 9706的抑制活性。方法采用正交实验法优化兖州卷柏水提物的提取效率,用比色法测定其总抗氧化活性,噻唑蓝（MTT）法研究水提物对人食管癌细胞的抑制作用。结果兖州卷柏水提物提取最佳工艺是质量体积 10 mL·g－1,水浴温度80 ℃,水浴时间20 min;随着浓度升高,其水提物的总抗氧化能力升高;对人食管癌细胞生长抑制作用随其水提物浓度和时间增加而增加。结论兖州卷柏水提物具有一定的抗氧能力,能体外抑制人食管癌细胞的生长。     

藤茶双氢杨梅树皮素对人肝癌BEL-7404细胞增殖的抑制作用

目的：探讨藤茶双氢杨梅树皮素（APS）的抗肿瘤作用。方法：以MTT法、生长曲线法、克隆形成法观察APS对人肝癌BEL-7404细胞的体外抑制作用。结果：MTT法中，APS对BEL-7404细胞的IC50为22．99μg／mL；细胞生长曲线法提示其对BEL-7404细胞生长有明显抑制作用；克隆形成法中，药物浓度在9．88μg／mL以上时抑制率为100％，药物浓度为6．58μg／mL时抑制率为69．65％。结论：APS对BEL-7404细胞的增殖有明显的抑制作用。     

Antitumor and antimetastatic activities of grape skin polyphenols in a murine model of breast cancer

Treatment modalities are not effective once breast cancer metastasis has occurred. Dietary botanicals may have a better protective effect. We therefore investigated the effects of grape skin polyphenols on a highly metastatic mouse mammary carcinoma cell line. In vitro treatment of 4T1 cells, with grape skin polyphenols resulted in inhibition of the migration and viability in a dose-dependent manner. The migration of 4T1 cells was significantly inhibited by grape skin polyphenols, even at a very low concentration (5 μg/ml), and was totally inhibited when the concentration was 20 μg/ml. However, 20 μg/ml of grape skin polyphenols inhibited cell viability by only 11.4%. The inhibition of migration is independent of decreased cell viability or apoptosis induction. Further analysis indicated that the inhibition of migration by grape skin polyphenols is involved in blocking the PI3k/Akt and MAPK pathways. The effects of dietary grape skin polyphenols were then examined using an in vivo model in which 4T1 cells were implanted subcutaneously in Balb/c mice. The metastasis of tumor cells to the lungs was inhibited significantly by dietary grape skin extracts (0.5 and 1.0 mg/ml in drinking water) and the survival of the mice enhanced. These data suggest that grape skin polyphenols possess chemotherapeutic efficacy against breast cancer with metastases.     

Inhibition of tumor cell invasiveness by chemically modified tetracyclines

COLO 205 is a cell line derived from a human colon carcinoma with high degradative activity towards extracellular matrix (ECM). It has been shown that COLO 205 cells produce matrix metalloproteinases (MMPs). MMPs are a family of enzymes known to degrade components of the ECM and have been implicated in tumor invasion. In the present study, we have analyzed the multiple effects of chemically modified tetracyclines (CMTs) on the expression and activity of MMPs secreted by COLO 205 cells in vitro with the aim of evaluating these compounds for potential use in management of invasive tumors. Because COLO 205 cells can degrade an interstitial ECM in serum-free medium in vitro, we have been able to compare the effects of the tetracyclines on this measure of invasive activity with their effects on proteinase expression and activity. We demonstrate here that one of the chemically modified tetracyclines, 6-deoxy-6-demethyl-4-de(dimethylamino)tetracycline (CMT-3) can effectively inhibit ECM degradation mediated by COLO 205 cells or their conditioned medium. Gelatin zymography and immunoblots show that CMT-3 has the ability to inhibit release of MMP-2 into conditioned medium as well as to inhibit MMP-2 gelatinolytic activity, which correlates with the results from ECM degradation assays. On the basis of our findings with COLO 205 cells we have expanded our evaluation of the tetracyclines to include effects on a genetically engineered line of MDA-MB-231 breast tumor cells overexpressing MMP-9 at levels over tenfold those of the parent cell line, and on three human prostate tumor cell lines, LNCaP, DU-145, and PC-3. We show here that CMT-3 displays multiple modes of action: inhibiting MMP activity, reducing levels of MMP expression, and exhibiting selective cytotoxicity towards some of the tumor cell lines.     

In vivo toxicity and antitumor activity of mangosteen extract

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.     

Anti-cancer effect of bee venom toxin and melittin in ovarian cancer cells through induction of death receptors and inhibition of JAK2/STAT3 pathway

We investigated whether bee venom and melittin, a major component of bee venom, inhibit cell growth through enhancement of death receptor expressions in the human ovarian cancer cells, SKOV3 and PA-1. Bee venom (1-5 μg/ml) and melittin (0.5-2 μg/ml) inhibited the growth of SKOV3 and PA-1 ovarian cancer cells by the induction of apoptotic cell death in a dose dependent manner. Consistent with apoptotic cell death, expression of death receptor (DR) 3 and DR6 was increased in both cancer cells, but expression of DR4 was increased only in PA-1 cells. Expression of DR downstream pro-apoptotic proteins including caspase-3, 8, and Bax was concomitantly increased, but the phosphorylation of JAK2 and STAT3 and the expression of Bcl-2 were inhibited by treatment with bee venom and melittin in SKOV3 and PA-1 cells. Expression of cleaved caspase-3 was increased in SKOV3, but cleaved caspase-8 was increased in PA-1 cells. Moreover, deletion of DR3, DR4, and DR6 by small interfering RNA significantly reversed bee venom and melittin-induced cell growth inhibitory effect as well as down regulation of STAT3 by bee venom and melittin in SKOV3 and PA-1 ovarian cancer cell. These results suggest that bee venom and melittin induce apoptotic cell death in ovarian cancer cells through enhancement of DR3, DR4, and DR6 expression and inhibition of STAT3 pathway.