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糖皮质激素治疗血管瘤的实验研究
作者姓名:Yu S  Liu WY  Tang YM  Wei T
作者单位:610041,成都,四川大学华西医院小儿外科
基金项目:国家教育部博士点基金资助项目(0040205102022),四川省科技厅资助项目(0040205301055)
摘    要:目的 探讨糖皮质激素治疗血管瘤的相关机制。方法 以裸鼠为载体,将婴幼儿增生期毛细血管瘤标本剪成小块转种于裸鼠皮下。转种后第45天随机分成两组:曲安缩松组的每个瘤体瘤内注射曲安缩松0 .05ml(4mg/ml),生理盐水组的每个瘤体瘤内注射生理盐水0. 05ml。于注射前当天、注射后第3天、1、2周观察移植血管瘤变化,检测糖皮质激素受体、血管内皮细胞生长因子、细胞增殖核抗原Ki -67的表达。结果 移植血管瘤瘤内注射曲安缩松后,大多数瘤体迅速在2周内消退,而生理盐水组瘤体继续生长,光镜及透射电子显微镜观察均显示血管瘤处于消退状态。注射曲安缩松后,移植血管瘤糖皮质激素受体、血管内皮细胞生长因子、Ki- 67表达明显减弱。瘤糖皮质激素受体阳性颗粒积分光密度在注射后第3天、注射后1、2周与注射前及同期生理盐水组比较差异有统计学意义(8044±585比495±48;P<0 .05,P<0. 01)。血管内皮细胞生长因子阳性颗粒积分光密度在注射后第3天、注射后1周、注射后2周与注射前及同期生理盐水组比较差异有统计学意义(8499±1336比407±76;P<0. 05,P<0 .01)。细胞增殖核抗原Ki- 67注射后2周与注射前及同期生理盐水组比较比较差异有统计学意义(8919±2810比399±46;P<0. 01)。糖皮质激素受体与血管内皮细胞生长因子及Ki

关 键 词:糖皮质激素治疗  血管内皮细胞生长因子  实验研究  糖皮质激素受体  抗原Ki-67  生理盐水组  外源性糖皮质激素  血管内皮细胞增殖  Ki-67表达  曲安缩松  积分光密度  瘤内注射  0.05  注射后  毛细血管瘤  统计学  相关机制  移植血管

An experimental study on the mechanism of therapy for hemangioma with glucocorticoid
Yu S,Liu WY,Tang YM,Wei T.An experimental study on the mechanism of therapy for hemangioma with glucocorticoid[J].National Medical Journal of China,2005,85(16):1121-1124.
Authors:Yu Song  Liu Wen-ying  Tang Yun-man  Wei Ting
Institution:Department of Pediatric Surgery, West China Hospital of Sichuan University, Chengdu 610041, China.
Abstract:OBJECTIVE: To observe the effect of intralesional administration of triamcinolone acetonide on the graft hemangioma in nude mouse and to explore the mechanism of glucocorticoid intervention. METHODS: The specimen of proliferating hemangioma from a male infant of 2 months old was obtained by surgery. The tissue was cut into small pieces 5 mm x 4 mm x 3 mm in size and grafted onto nude mice subcutaneously. Triamcinolone acetonide was administered intralesionally at 45th day after graft. Grafted specimens were taken before and at 3rd day, 1st week, and 2nd week after triamcinolone acetonide administration. In mice of control group, introlesional injection of the same volume of normal saline was given. Glucocorticoid receptor (GR), Vascular endothelial growth factor (VEGF) and Ki-67 were detected. RESULTS: Significant decrease of graft volume was observed in the experimental group compared to that in control group, and the grafts in experimental group turned harden and whitish in 2 weeks. Under microscopy, grafts of experimental group were mainly composed of lipofibrous tissue. Collapse and blockage of vascular lumens were frequent. While control grafts involved large amount of proliferative capillaries and signs of destruction was not observed. With administration of triamcinolone acetonide injection, the stainings of GR, VEGF, and Ki-67 turned weaker significantly. Significant differences of GR, VEGF, and Ki-67 staining were obtained between experimental group and control group, and between experimental group and normal subcutaneous tissue group. After intralesional administration of triamcinolone acetonide, the coefficient correlations of GR to VEGF and to Ki-67 were 0.766 (P < 0.01) and 0.643 (P < 0.01), respectively. The coeffecient correlation of VEGF to Ki-67 was 0.567 (P < 0.05). CONCLUSION: The effect of external glucocorticoid on hemangioma might be mediated by GR, i.e., glucocorticoid binds to it is specific receptor and forms a glucocorticoid-GR complex, and the complex interacts with glucocorticoid response element in target gene, and then inhibit secretion of VEGF. With decreased VEGF secretion, proliferation of endothelial cells is hampered and the hemangioma involutes.
Keywords:Hemangioma  Nude mice  Glucocorticoids  Glucocorticoid receptor  Vascular endothelial growth factor
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