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1.
树突状细胞是体内专职的抗原提呈细胞,具有摄取、处理和呈递抗原至T细胞的功能。同时,DC是体内进行交叉激活的主要抗原提呈细胞,可以使外源性肿瘤抗原激活CTL从而杀伤肿瘤细胞。文章从肿瘤细胞对于DC在不同阶段的抑制作用以及DC对于肿瘤细胞的杀伤作用两方面列举DC与肿瘤细胞相互关系的研究近况,以说明DC在肿瘤治疗中的重要作用。  相似文献   

2.
西黄丸对细胞突变与肿瘤生长抑制的研究   总被引:3,自引:0,他引:3  
目的:探讨西黄丸的抗突变和抗肿瘤作用.方法:以小鼠骨髓细胞微核试验和睾丸染色体畸变实验观察西黄丸的抗突变作用;以S-180和H-22移植性肿瘤观察西黄丸的抗肿瘤作用.结果:西黄丸对环磷酰胺诱发的小鼠骨髓细胞微核和丝裂霉素诱发的小鼠睾丸细胞染色体畸变均有明显的抑制效果;对S-180和H-22小鼠移植性肿瘤生长有明显的抑制作用.结论:西黄丸对体细胞和生殖细胞的DNA损伤均有较好的保护作用;对小鼠移植性肿瘤较好的抑瘤作用.  相似文献   

3.
以Neuro-2a细胞为体外神经分化细胞模型,观察多穗柯乙醇提取物(EELP)对Neuro-2a细胞分化的影响.实验结果表明,EELP可能通过激活Erk1/2和Akt信号通路,显著提高Neuro-2a细胞的分化率,同时促进神经突的生长.该研究可为多穗柯甜茶在神经系统疾病治疗和保健方面的应用提供重要实验依据.  相似文献   

4.
本文以MTT法考察菊叶中总黄酮的体外抗肿瘤活性;以小鼠移植瘤模型测定总黄酮对荷瘤小鼠抑瘤率和腹腔巨噬细胞吞噬能力,研究其体内抗肿瘤活性和免疫调节作用.结果表明,总黄酮对S180细胞生长有显著抑制作用.体内试验表明,与生理盐水组相比,总黄酮对小鼠S180实体瘤有显著抑制作用(P〈0.01),抑瘤同时可促进体重增长;总黄酮高剂量组可提高荷瘤小鼠的脾指数和胸腺指数.与环磷酰胺组和生理盐水组比较,总黄酮可使荷S180实体瘤小鼠腹腔巨噬细胞吞噬能力升高,表明其对小鼠没有免疫抑制作用.  相似文献   

5.
纯化伤寒杆菌HSP70,观察其对小鼠S180肿瘤细胞的抑制作用,对荷瘤小鼠连续皮下注射伤寒杆菌HSP70,每只小鼠每天注射100μ/mL,的伤寒杆菌HSP70.5mL,每天一次.9天后处死小鼠,剥离肿瘤,分别称量实验组与对照组小鼠肿瘤的重量.结果表明,伤寒杆菌HSP70能明显抑制小鼠S180肿瘤细胞在小鼠体内的生长.  相似文献   

6.
目的:研究鹅绒委陵菜多糖(PAP)的抗肿瘤作用及其免疫调节作用。方法:用小鼠肝癌(S180)移植肿瘤的动物模型,以肿瘤抑制率、溶血素、NK细胞活性和淋巴细胞增殖率作指标,结果表明,鹅绒委陵菜多糖不仅能显著抑制移植性肿瘤S180的生长,而且还能明显促进荷瘤鼠的体液免疫和提高荷瘤鼠的脾细胞转化功能及增强NK细胞活性,均以200mg。kg-1.d-1效果最佳。结论:鹅绒委陵菜多糖的抗肿瘤作用和其免疫调节作用有明显的相关性,鹅绒委陵菜多糖的抗肿瘤作用可能与激活体内免疫系统有关。  相似文献   

7.
为解决肿瘤个体化治疗中体内外模型差异的问题,明晰体外模型对药敏检测的影响。实验在体外建立肿瘤3D细胞模型,通过ATP生物荧光法(ATP-TCA)检测3D肿瘤细胞中ATP的含量,间接反映3D肿瘤细胞对化疗药物5-FU和紫杉醇的敏感性。同时,通过Live/Dead细胞成像实验进一步研究化疗药物对3D肿瘤细胞的杀伤作用。研究发现化疗药物5-FU和紫杉醇均可抑制HepG2和A549肿瘤3D细胞的生长,且紫杉醇对HepG2 3D细胞的抑制作用明显强于5-FU。药物敏感性评价结果显示,HepG2 3D细胞对化疗药物紫杉醇中度敏感,对5-FU不敏感。A549 3D细胞对紫杉醇和5-FU均中度敏感。Live/Dead细胞成像结果进一步证实了PTX对HepG2 3D细胞具有明显的毒性。本实验为体外药敏检测提供了新思路。  相似文献   

8.
目的:探讨中药复肝春6号(Fuganchun 6,FGC-6)诱导小鼠肝癌H22细胞凋亡的机理.方法:将FGC-6制成水煎剂,过滤,最后用微孔滤膜过滤除菌.药物浓度以生药计.采用MTT法计算FGC-6对H22细胞的半数致死量浓度和琼脂糖凝胶电泳对药物诱导的凋亡细胞进行DNA ladder分析,流式细胞术检测药物作用下的细胞凋亡率和细胞周期时相变化,透射电镜检测凋亡细胞超微结构的变化.结果:FGC-6对H22细胞的半数致死量浓度为240mg/mL.DNA ladder分析药物组可见明显的凋亡梯状条带.FGC-6作用下的小鼠H22肝癌细胞周期时相发生变化,随药物浓度的增加细胞凋亡率明显上升.透射电镜下FGC-Ⅰ组细胞具有明显的坏死特征.FGC-Ⅱ组肿瘤细胞可见明显的凋亡特征.结论:复肝春6号可以使体外培养的H22细胞染色体DNA断裂,阻滞在细胞周期的G1/G0 期,使H22细胞的超微结构改变等途径诱导细胞凋亡.  相似文献   

9.
为了探讨光敏剂疗内注射法在临床上的应用,本实验将高浓度血卟啉衍生物直接注入荷瘤小鼠的肿瘤内,利用组织涂片法,通过荧光显微镜观察。结果,注射后1-5天内,局部注射组肿瘤内发橘红色荧光的细胞的百分比明显高于腹腔注射组,以1-4天为著.  相似文献   

10.
目的:观察姜黄素提取物体外对流感病毒H1N1、H3N2的抑制作用。方法:用狗肾细胞(MDCK)观察姜黄素体外对A型流感病毒H1N1亚型、A型流感病毒H3N2亚型病毒的直接杀灭作用。结果:姜黄素最大无毒浓度为12.5g/L,对H1N1有效抑制浓度为6.25g/L,对H3N2有效抑制浓度为1.56g/L。结论:姜黄素提取物确有明显的抗H1N1、H3N2复制作用。  相似文献   

11.
Objective: To investigate the in-vitro antitumor immune responses of dendritoma formed by mouse hepatocellular carcinoma (HCC) cells and lymphotactin (Lptn) gene modified dendritic cells (DCs). Method: DCs prepared from mouse bone marrow were genetically modified by lymphotactin adenovirus, and fused with H22 cells by polyethylene glycol (PEG). RT-PCR and ELISA were employed to identify lymphotactin expression at mRNA and protein level. Cell phenotypes and fusion efficiency was detected by FACS. The stimulatory effect of DC on T cells was detected by mixed lymphocyte reaction. The cytotoxicity activity against H22 cells was assayed by LDH method. Results: Lymphotactin could be efficiently expressed by DCLptn/H22 hybridoma. DCLptn/H22 cells could induce potent T cell proliferation effect and generate strong cytotoxic T lymphocyte (CTL) reaction against allogenic H22 cells. Conclusion: Lymphotactin genetic modification could enhance the in vitro immune activity of the dendritoma.  相似文献   

12.
目的研究不同剂量反应停及反应停协同环磷酰胺对小鼠荷瘤H22(肝癌)实体型肿瘤的影响。方法建立小鼠肝癌移植实体型肿瘤模型,比较不同剂量反应停对小鼠肝癌的影响,同时观察反应停协同环磷酰胺对小鼠肝癌的影响。通过研究反应停对小鼠迟发型变态反应的影响探究其免疫作用。结果反应停对小鼠荷瘤H22呈现明显剂量依赖性抑制作用,反应停与环磷酰胺具有协同抗小鼠肝癌作用。反应停对小鼠迟发型变态反应呈剂量依赖性促进作用。结论反应停具有抗肝癌作用,而且与环磷酰胺具有协同抗肿瘤作用,此作用与反应停抗免疫作用有关。  相似文献   

13.
为研究螺旋藻的免疫调节及抗肿瘤作用的有效成份,增强药物作用效应,通过煮沸及高压,获得螺旋藻的耐热成份.将处理后的螺旋藻,皮下注射给腹腔荷小鼠肝癌细胞H22瘤株的荷瘤小鼠,同时设立生理盐水对照组.共给药4次,记录误组荷瘤小鼠成活天数.实验结束后,再重复一次本试验.实验结果表明:实验治疗组小鼠,平均成活天数,第一次实验及第二次实验分别为19天及18.9天,(P>0.05).对照组两次实验结果分别为15.8天和15.9天(P>0.05).说明实验稳定可靠.统计学处理表明,实验治疗组与对照组小鼠,存活天数有极显著差异P<0.01,提示螺旋藻的耐热成份,对肿瘤有一定的治疗作用.  相似文献   

14.
Distribution of H.pylori antigens in gastric mucosa and its significance   总被引:2,自引:0,他引:2  
INTRODUCTION Helicobacter pylori (H.pylori) was grouped as a class I carcinogen by the International Agency for Research on Cancer in 1994. A direct relation be-tween H.pylori infection and gastric carcinogenesis was demonstrated in 1998 in an experimental animal model (Watanabe et al., 1998). However, the role of H.pylori in human gastric carcinogenesis is sup-ported almost exclusively by epidemiological data and prospective histopathological studies. So far the mechanism of H.pylor…  相似文献   

15.
Objective: To investigate the distribution of H. pylori antigens in the gastric mucosa in patients with H. pylori infection, and the relationship between the distribution and gastric cancer. Methods: Of 112 patients confirmed by pathological study to have chronic superficial gastritis, precancerous changes (chronic atrophic gastritis, intestinal metaplasia or atypical hyperplasia) and gastric cancer, 28 were H. pylori negative and 84 were H. pylori positive. H. pylori antigens in the gastric mucosa were detected by immunohistochemistry. Results: The H. pylori positive group, comprised 12 of 22 (50.0%) in the chronic superficial gastritis group, 22 of 25 (88.0%) in the precancerous changes group and 13 of 35 (37.1%) in the gastric cancer group. The positive rates of H. pylori antigens in the cytoplasm progressively increased, respectively at 0.0% (0/12),63.6% (14/22) and 84.6% (11/13) for the same groups (χ2=19.76, P=0.000); H.pylori antigens were located in the mucus layer and above the neck of the mucosal gland in 9 of 12 (75.0%) cases with chronic superficial gastritis, at the neck of the mucosal gland and the isthmus in 12 of 22 (54.5%) cases with precancerous changes, below the isthmus in 9 of 13 (69.2%) cases with gastric cancer (x2=25.30, P=0.000). In the H. pylori negative group, no H.pylori antigen was observed. Conclusion: With the progression of chronic superficial gastritis→precancerous changes→gastric cancer, H. pylori antigens progressively migrated from the outer part to the inner part of the cell, and from the superficial to the deep gastric mucosa.  相似文献   

16.
Objective: To investigate the distribution ofH. pylori antigens in the gastric mucosa in patients withH. pylori infection, and the relationship between the distribution and gastric cancer. Methods: Of 112 patients confirmed by pathological study to have chronic superficial gastritis, precancerous changes (chronic atrophic gastritis, intestinal metaplasia or atypical hyperplasia) and gastric cancer, 28 wereH. pylori negative and 84 wereH. pylori positive.H. pylori antigens in the gastric mucosa were detected by immunohistochemistry. Results: TheH. pylori positive group, comprised 12 of 22 (50.0%) in the chronic superficial gastritis group, 22 of 25 (88.0%) in the precancerous changes group and 13 of 35 (37.1%) in the gastric cancer group. The positive rates ofH. pylori antigens in the cytoplasm progressively increased, respectively at 0.0% (0/12), 63.6% (14/22) and 84.6% (11/13) for the same groups (χ 2=19.76,P=0.000);H. pylori antigens were located in the mucus layer and above the neck of the mucosal gland in 9 of 12 (75.0%) cases with chronic superficial gastritis, at the neck of the mucosal gland and the isthmus in 12 of 22 (54.5%) cases with precancerous changes, below the isthmus in 9 of 13 (69.2%) cases with gastric cancer (χ 2=25.30,P=0.000). In theH. pylori negative group, noH. pylori antigen was observed. Conclusion: With the progression of chronic superficial gastritis→precancerous changes→gastric cancer,H. pylori antigens progressively migrated from the outer part to the inner part of the cell, and from the superficial to the deep gastric mucosa.  相似文献   

17.
The effect of ginsenosides on proliferation of type A spermatogonia was investigated in 7-day-old mice.Spermatogonia were characterized by c-kit expression and cell proliferation was assessed by immunocytochemical demonstration of proliferating cell nuclear antigen (PCNA).After 72-h culture,Sertoli cells formed a confluent monolayer to which numerous spermatogonial colonies attached.Spermatogonia were positive for c-kit staining and showed high proliferating activity by PCNA expression.Ginsenosides (1.0~10 μg/ml) significantly stimulated proliferation of spermatogonia.Activation of protein kinase C (PKC) elicited proliferation of spermatogonia at 10-8 to 107 mol/L and the PKC inhibitor H7 inhibited this effect.Likewise,ginsenosides-stimulated spermatogonial proliferation was suppressed by combined treatment of H7.These results indicate that the proliferating effect ofginsenosides on mouse type A spermatogonia might be mediated by a mechanism involving the PKC signal transduction pathway.  相似文献   

18.
19.
合成了3种季铵盐型阳离子表面活性荆(C16H33)2N(CH3)2Br(双十六烷基二甲基溴化铵),C16H33,NC33H45(CH3)2Br(二十二烷基十六烷基二甲基溴化铵),C16H33NC12H25(CH3)2Br(十六烷基十二烷基二甲基溴化铵),并考察了其对水/有机两相体系中苯甲醛与苯乙酮Aldol缩合反应性能的影响.结果显示,含有两条疏水长链的阳离子表面活性剂对水/有机两相体系中苯甲醛与苯乙酮Aldol缩合反应具有明显的加速作用,其催化活性明显高于其它类型的表面活性剂;结果还显示,阳离子表面活性剂分子中疏水碳链的数目增加、疏水碳链的增长均有利于Aldol缩合反应.  相似文献   

20.
目的:通过丹参七种水溶性有效成分多水平均匀设计配伍的血管内皮细胞保护作用筛选研究,评价中药有效成分的均匀设计-高通量筛选技术(uniform design-high throughput screening,UD-HTS)的应用.方法:选取原儿茶醛、原儿茶酸、咖啡酸、丹参素钠、迷迭香酸、丹酚酸A、丹酚酸B七种丹参水溶性单体有效成分七个水平(1×10-4~1×10-10 mol·L-1)进行均匀设计配伍组合,通过H2O2诱导的氧化应激损伤血管内皮细胞模型、血管内皮细胞营养剥夺模型评价各种有效成分配伍组合对药效的影响.结果:经过初筛和复筛,初步得到了2个最佳配伍组合样品(A2、B4),其细胞存活率分别为(70±4)%,(76±3)%.不同的细胞损伤模型筛选出不同的最优配比.结论:均匀设计配伍与中药复方配伍有相似之处,均匀设计-高通量筛选技术是适用于传统多因素多水平组合特点的大规模药效筛选研究新方法.  相似文献   

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