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E1B-55KD基因缺陷腺病毒联合热疗对肿瘤的治疗作用

Effect of E1B-55KD Gene Defect Adenovirus Combined with Thermotherapy on Tumor
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摘要 目的:通过基因治疗与温热治疗方法相结合,观测两者治疗手段是否有协同作用。方法:将40只荷瘤小鼠随机分为4组,A组:E1B-55KD基因缺陷腺病毒感染组;B组:温热治疗组;C组:E1B-55KD基因缺陷腺病毒感染+温热治疗组;D组:空白对照组。治疗前后测量瘤体直径,实验前后取瘤体称重;Western蛋白分析对HSP进行定位、定量检测;流式细胞仪进行T细胞亚群检测,计算CD3+、CD4+、CD8+细胞含量,CD4+/CD8+值。结果:(1)A、B、C组肿瘤体积较D组均有减少,提示与对照组相比,各治疗组均有不同程度的肿瘤抑制作用,而C组小鼠肿瘤生长受抑最为明显。(2)A、B、C组瘤重分别与D组比较,结果均有减少,其中C组减少最为明显。(3)B、C两组小鼠肿瘤组织经加热后,细胞浆内的热休克蛋白较未加热的A、D两组明显增加。(4)A、B、C组与D组相比较CD8(CTL)均有提高,而以C组t最为显著,提示联合治疗组对CTL增殖的刺激作用更加显著。结论:E1B-55KD基因缺陷腺病毒联合热疗对肿瘤的治疗有协同作用。 Objective: To investigate synergistic effect of gene therapy combined with thermotherapy. Methods: Fourty tumorbearing mice were randomly divided into 4 groups: A group (infected by E1 B-55 KD gene defect adenovirus), B group (treated by thermotherapy) , C group (infected by E1B-55KD gene defect adenovirus and treated by thermotherapy) , D group (control). The tumour's diameter and weight were mearsued before and after the experiment; the HSP were located and quantitated by Western blot; the T cell subgroup were detected by flow cytometry and the content of CD3^+, CD4^+ , CD8^+, CD4^+/CD8^+ were calculated. Re. stilts: (1) Compared with D group, tumor in all therapy group were depressed, which in C group was restrained extremely. (2) Compared with D group, the weight of tumor was reduced in A, B, C group, among them C group reduced significantly. (3) By heating the tumor, the HSP of cytolymph was obviously increased in B, C group, but which not occurred in A, D group. (4) Compared with D group, CD8 (CTL)was elevated in A, B, C group; among them C group elevated significantly; all these reflect that therapeutic alliance had more promoting effect on the generation of CTL. Conclusion: E1B-55KD gene defect adenovirus combined with therrnotherapy has synergistic healing effect on tumor.
出处 《沈阳医学院学报》 2009年第3期148-150,共3页 Journal of Shenyang Medical College
关键词 E1B-55KD基因 腺病毒 热疗 热休克蛋白 E1B-55KD gene adenovirus thermotherapy heat shock protein
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  • 1Lisa Y. Zhao, Aleixo Santiago, Jilin Liu, et al. Repression of p53-mediated transcription by adenovirus E1B 55-kDa does not require corepressor mSin3A and histone deacetylases [ J]. Biol Chem, 2007, 282:7001-7010. 被引量:1
  • 2Heisec, Sampson-Johannes A, William A, et al. ONYX-015, an E1B gene-attenuated adenovirus, cause tumor specific cytolysis and antitumoral efficacy that can be augmented by standard chemotherapeutic agents [J]. Nat Med, 1997, 3 (6): 639-645. 被引量:1
  • 3Rogulski KR, Freytag SC, Zhang K, et al. In vivo antitunor activity of ONYX-015 is influenced by p53 status and is augmented by radiotherapy [J]. Cancer Res, 2000, 60 (5): 1193-1196. 被引量:1
  • 4Wu F, Wang ZB, Lu P, et al. Activated anti-tumor immunity in cancer patients after high intensity focused ultrasound solution [J]. Ultrasound Med Biol, 2004, 30 (9): 1217-1222. 被引量:1
  • 5王旭霞,张盈华,郝晓柯,殷缨,陶秦渝.胃癌患者红细胞免疫功能及T淋巴细胞亚群的变化[J].肿瘤防治杂志,2003,10(5):493-495. 被引量:8
  • 6Stawarz B, Zielinske H, Szm Ingielski S, et al. Transrectal hyperthem in as palliative for advanced adenocarc inom a of prostate and studies of cell-mediated immunity [ J ]. Urology, 1993, 41 (6) : 548 -553. 被引量:1
  • 7Harada M, Kimura G, Nomoto K. Heat shock protein and the antitumor T cell response [ J]. Biotherapy, 1998, 10:B229 -235. 被引量:1
  • 8Prohaszka Z, Singh M, Nagy K, et al. Heat shock protein 70 is a potent activator of the human complement system [ J ]. Cell Stress Chaperones, 2002, 7 (1): 117-122. 被引量:1

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