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目的:评估应用高压氧治疗前列腺癌放疗后出血性膀胱炎的安全性,探讨高压氧对体内前列腺癌细胞生长的影响。方法:采用人前列腺癌LNCaP细胞株皮下接种构建小鼠荷瘤模型(n=30),随机分为对照组(n=15)和实验组(n=15)。对照组常压常氧条件下饲养,实验组每周进行5次0.2MPa高压氧暴露,共计20次。连续观察4周两组移植瘤生长体积的变化,应用免疫组化法比较两组瘤体组织相关病理学特征指标:瘤体微血管密度(CD34)、瘤细胞增殖(Ki-67蛋白)以及瘤细胞凋亡(p53、p27蛋白)。结果:肿瘤接种后第28天,对照组移植瘤体积为(122.0±8.2)mm3,实验组为(120.0±7.9)mm3,两组差异无显著性(P>0.05);对照组移植瘤CD34及Ki-67、p53、p27蛋白表达的阳性细胞率分别为(36.2±4.9)%、(75.3±8.4)%、(44.2±5.7)%、(61.5±5.5)%,实验组分别为(39.3±5.2)%、(78.1±7.6)%、(40.4±6.2)%、(63.7±5.1)%,病理学特征均无显著性差异(P>0.05)。结论:高压氧对小鼠荷瘤模型前列腺癌细胞生长无促进作用,对前列腺癌中新生血管也无明显影响。
OBJECTIVE: To assess the safety of hyperbaric oxygen in the treatment of hemorrhagic cystitis after radiotherapy of prostate cancer and to investigate the effect of hyperbaric oxygen on the growth of prostate cancer cells in vivo. Methods: The mouse tumor-bearing model (n = 30) was established by subcutaneous inoculation of human prostate cancer cell line LNCaP. The mice were randomly divided into control group (n = 15) and experimental group (n = 15). The control group was fed under normobaric conditions. The experimental group was exposed to 0.2MPa hyperbaric oxygen for 5 times per week for a total of 20 times. The growth volume of the transplanted tumor in two groups was observed continuously for 4 weeks. Immunohistochemical method was used to compare the pathological features of the two groups: tumor microvessel density (CD34), tumor cell proliferation (Ki-67 protein) and tumor cells Apoptosis (p53, p27 protein). Results: The tumor volume of the control group was (122.0 ± 8.2) mm3 on the 28th day after tumor inoculation, and (120.0 ± 7.9) mm3 in the experimental group. There was no significant difference between the two groups (P> 0.05) The positive cell rates of Ki-67, p53 and p27 were (36.2 ± 4.9)%, (75.3 ± 8.4)%, (44.2 ± 5.7)% and (61.5 ± 5.5)%, respectively 5.2%, 78.1 ± 7.6%, 40.4 ± 6.2% and 63.7 ± 5.1%, respectively. There was no significant difference in pathological features (P> 0.05). CONCLUSION: Hyperbaric oxygen has no effect on the growth of prostate cancer cells in mice bearing tumor model, and has no obvious effect on the neovascularization in prostate cancer.