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首页> 外文期刊>World Journal of Gastroenterology >Inhibitory effect of arsenic trioxide on angiogenesis and expression of vascular endothelial growth factor in gastric cancer.
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Inhibitory effect of arsenic trioxide on angiogenesis and expression of vascular endothelial growth factor in gastric cancer.

机译：三氧化二砷对胃癌血管生成和血管内皮生长因子表达的抑制作用。

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AIM: To investigate the inhibitory effect of As(2)O(3) on angiogenesis of tumor and expression of vascular endothelial growth factor (VEGF) in tumor cells in vivo and in vitro. METHODS: The solid tumor model was formed in nude mice with the gastric cancer cell line SGC-7901. The animals were randomly divided into three groups. As(2)O(3) was injected into the arsenic-treated groups (2.5 mg/kg and 5 mg/kg) and the same volume of saline solution was injected into the control group. Microvessel density (MVD) and expression of VEGF were detected with immunofluorescence laser confocal technology. Further expression of VEGF protein and VEGF mRNA was measured with Western bloting and fluorescence quantitative RT- PCR in SGC-7901 cells treated with As(2)O(3). RESULTS: In nude mice, after treatment with 5 mg/kg and 2.5 mg/kg As(2)O(3) respectively, about 50% and 30% tumor growth inhibition were observed correspondingly (P<0.05, P<0.05). Decrease in MVD appeared in As(2)O(3)-treated tumors compared with control group (P<0.001, P<0.001). MVD in tumors was significantly lower in 5 mg/kg group than in 2.5 mg/kg group (P<0.01). The fluorescence intensity levels of VEGF in tumor cells were significantly lowered in the arsenic-treated groups (P<0.01, P<0.01). The fluorescence intensity level of VEGF in 5 mg/kg group was lower than that in 2.5 mg/kg group (P<0.01). In vitro, the expression of VEGF protein decreased in dose- and time-dependent manner after the treatment with As(2)O(3), but in VEGF mRNA no significant difference was found between the control group and the treated groups. CONCLUSION: As(2)O(3) can inhibit solid tumor growth by inhibiting the formation of new blood vessels. One of the mechanisms is that As(2)O(3) can inhibit VEGF protein expression.
机译：目的：探讨As（2）O（3）在体内外对肿瘤血管生成和肿瘤细胞中血管内皮生长因子（VEGF）表达的抑制作用。方法：利用胃癌细胞系SGC-7901在裸鼠体内建立实体瘤模型。将动物随机分为三组。将As（2）O（3）注入砷处理组（2.5 mg / kg和5 mg / kg），并将相同体积的盐溶液注入对照组。用免疫荧光激光共聚焦技术检测微血管密度（MVD）和VEGF的表达。用Western印迹和荧光定量RT-PCR在用As（2）O（3）处理的SGC-7901细胞中测量VEGF蛋白和VEGF mRNA的进一步表达。结果：在裸鼠中，分别用5 mg / kg和2.5 mg / kg As（2）O（3）治疗后，分别观察到约50％和30％的肿瘤生长抑制（P <0.05，P <0.05）。与对照组相比，经As（2）O（3）处理的肿瘤中MVD降低（P <0.001，P <0.001）。 5 mg / kg组的肿瘤MVD明显低于2.5 mg / kg组（P <0.01）。砷处理组肿瘤细胞中VEGF的荧光强度水平明显降低（P <0.01，P <0.01）。 5 mg / kg组的VEGF荧光强度低于2.5 mg / kg组（P <0.01）。在体外，用As（2）O（3）治疗后，VEGF蛋白的表达以剂量和时间依赖性方式降低，但在对照组和治疗组之间，VEGF mRNA的表达没有明显差异。结论：As（2）O（3）可通过抑制新血管的形成来抑制实体瘤的生长。机制之一是As（2）O（3）可以抑制VEGF蛋白的表达。

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