内皮抑素对裸鼠人舌鳞癌颈淋巴结转移模型的实验研究
发布时间：2019-02-22 18:49
【摘要】：研究目的：观察内皮抑素对人舌鳞癌肿瘤的生长、脉管生成及颈淋巴转移的影响,并对内皮抑素抑制脉管生成可能的机制进行分析。 研究方法：本研究应用Tca83舌鳞癌细胞系建立裸鼠舌癌原位移植模型,将裸鼠随机分为A、B、C共3组,分别给予A组皮下注射生理盐水0.1ml；B组皮下注射内皮抑素10mg/kg/d；C组皮下注射内皮抑素20mg/kg/d。每日注射药物一次,连续给予两周。观察舌癌动物模型肿瘤生长及淋巴转移特点,采用免疫组织化学方法标记病灶中的脉管。并检测VEGF-C的表达情况,计数病灶脉管密度及VEGF-C阳性率。采用SPSS20.0软件包对数据进行统计学分析。 结果：1、实验组裸鼠较对照组肿瘤生长减慢,实验结束时肿瘤体积A组为5.838±0.095mm3,B组为3.554±0.061mm3,C组为2.578±0.074mm3。内皮抑素对肿瘤生长具有抑制作用。进一步计算各组标本微血管密度,A组为10.4±1.26个/视野,B组为4.4±0.84个/视野,C组为2.2±0.79个/视野。内皮抑素对肿瘤血管生成具有抑制作用,且随剂量增加,抑制作用增强。 2、高剂量组裸鼠较对照组和低剂量组淋巴转移率低,A组为50%,B组为20%,C组为0%。高剂量内皮抑素对肿瘤淋巴转移具有抑制作用。进一步计算各组标本微淋巴管密度,A组为6.2±0.92个/视野,B组为4.0±1.05个/视野,C组为2.2±0.92个/视野。内皮抑素对肿瘤淋巴管生成具有抑制作用,且随剂量增加,抑制作用增强。 3、另外,A组VEGF-C阳性率为80%；B组VEGF-C阳性率为40%；C组VEGF-C阳性率为20%。高剂量内皮抑素可以下调肿瘤细胞VEGF-C的表达。 结论：1、肿瘤血管生成在肿瘤生长中发挥重要作用,内皮抑素可以抑制肿瘤血管生成,从而抑制肿瘤生长,且具有剂量依赖性,随浓度增加其抑制作用逐渐增强,但未见其缩小抑或消除肿瘤的作用。 2、肿瘤淋巴管生成在恶性肿瘤的侵袭转移过程中具有重要作用,高剂量内皮抑素可以抑制肿瘤淋巴管生成,从而抑制肿瘤淋巴转移。 3、内皮抑素可能是通过下调细胞VEGF-C的表达进而抑制肿瘤淋巴管生成。
[Abstract]:Aim: to observe the effects of endostatin on the growth, angiogenesis and cervical lymphatic metastasis of human tongue squamous cell carcinoma, and to analyze the possible mechanism of endostatin inhibiting angiogenesis. Methods: in this study, Tca83 tongue squamous cell carcinoma cell line was used to establish orthotopic transplantation model of tongue carcinoma in nude mice. Nude mice were randomly divided into 3 groups: group A was subcutaneously injected with normal saline 0.1 ml. Group B was subcutaneously injected with endostatin 10 mg / kg / d and group C was subcutaneously injected with 20 mg / kg / d endostatin. The drug was injected once a day for two weeks. To observe the characteristics of tumor growth and lymphatic metastasis in tongue cancer animal model and to label the vessels in the lesion by immunohistochemical method. The expression of VEGF-C, vascular density and positive rate of VEGF-C were measured. The data were analyzed by SPSS20.0 software package. Results: 1. The tumor growth of the nude mice in the experimental group was slower than that in the control group. At the end of the experiment, the tumor volume of group A was 5.838 卤0.095 mm ~ (3) and that of group B was 3.554 卤0.061 mm ~ (3) and that of group C was 2.578 卤0.074 mm ~ (3). Endostatin inhibits tumor growth. The microvessel density of group A was 10.4 卤1.26 / visual field, group B was 4.4 卤0.84 / visual field, group C was 2.2 卤0.79 / visual field. Endostatin has inhibitory effect on tumor angiogenesis, and the inhibitory effect is enhanced with the increase of dose. 2, the lymphatic metastasis rate of the nude mice in the high dose group was lower than that in the control group and the low dose group, and the lymph node metastasis rate in group A was 50 and that in group B was 20. High dose endostatin can inhibit lymphatic metastasis of tumor. The density of microlymphatic vessels in each group was 6.2 卤0.92 / visual field, 4.0 卤1.05 / visual field in group B and 2.2 卤0.92 / visual field in group C. Endostatin has inhibitory effect on lymphangiogenesis of tumor, and the inhibitory effect is enhanced with the increase of dose. In addition, the positive rate of VEGF-C in group A was 80 and the positive rate of VEGF-C in group B was 40. The positive rate of VEGF-C in group C was 20. High dose endostatin can down-regulate the expression of VEGF-C in tumor cells. Conclusion: 1. Tumor angiogenesis plays an important role in tumor growth. Endostatin can inhibit tumor angiogenesis and inhibit tumor growth in a dose-dependent manner. However, it has not been seen to shrink or eliminate the role of tumor. 2. Tumor lymphangiogenesis plays an important role in the invasion and metastasis of malignant tumor. High dose of endostatin can inhibit lymphangiogenesis of tumor and thus inhibit lymphatic metastasis of tumor. 3. Endostatin may inhibit lymphangiogenesis by down-regulating the expression of VEGF-C.
【学位授予单位】：天津医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R739.86
本文编号：2428506
[Abstract]:Aim: to observe the effects of endostatin on the growth, angiogenesis and cervical lymphatic metastasis of human tongue squamous cell carcinoma, and to analyze the possible mechanism of endostatin inhibiting angiogenesis. Methods: in this study, Tca83 tongue squamous cell carcinoma cell line was used to establish orthotopic transplantation model of tongue carcinoma in nude mice. Nude mice were randomly divided into 3 groups: group A was subcutaneously injected with normal saline 0.1 ml. Group B was subcutaneously injected with endostatin 10 mg / kg / d and group C was subcutaneously injected with 20 mg / kg / d endostatin. The drug was injected once a day for two weeks. To observe the characteristics of tumor growth and lymphatic metastasis in tongue cancer animal model and to label the vessels in the lesion by immunohistochemical method. The expression of VEGF-C, vascular density and positive rate of VEGF-C were measured. The data were analyzed by SPSS20.0 software package. Results: 1. The tumor growth of the nude mice in the experimental group was slower than that in the control group. At the end of the experiment, the tumor volume of group A was 5.838 卤0.095 mm ~ (3) and that of group B was 3.554 卤0.061 mm ~ (3) and that of group C was 2.578 卤0.074 mm ~ (3). Endostatin inhibits tumor growth. The microvessel density of group A was 10.4 卤1.26 / visual field, group B was 4.4 卤0.84 / visual field, group C was 2.2 卤0.79 / visual field. Endostatin has inhibitory effect on tumor angiogenesis, and the inhibitory effect is enhanced with the increase of dose. 2, the lymphatic metastasis rate of the nude mice in the high dose group was lower than that in the control group and the low dose group, and the lymph node metastasis rate in group A was 50 and that in group B was 20. High dose endostatin can inhibit lymphatic metastasis of tumor. The density of microlymphatic vessels in each group was 6.2 卤0.92 / visual field, 4.0 卤1.05 / visual field in group B and 2.2 卤0.92 / visual field in group C. Endostatin has inhibitory effect on lymphangiogenesis of tumor, and the inhibitory effect is enhanced with the increase of dose. In addition, the positive rate of VEGF-C in group A was 80 and the positive rate of VEGF-C in group B was 40. The positive rate of VEGF-C in group C was 20. High dose endostatin can down-regulate the expression of VEGF-C in tumor cells. Conclusion: 1. Tumor angiogenesis plays an important role in tumor growth. Endostatin can inhibit tumor angiogenesis and inhibit tumor growth in a dose-dependent manner. However, it has not been seen to shrink or eliminate the role of tumor. 2. Tumor lymphangiogenesis plays an important role in the invasion and metastasis of malignant tumor. High dose of endostatin can inhibit lymphangiogenesis of tumor and thus inhibit lymphatic metastasis of tumor. 3. Endostatin may inhibit lymphangiogenesis by down-regulating the expression of VEGF-C.
【学位授予单位】：天津医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R739.86
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