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目的:观察姜黄素对原发性肝癌模型大鼠组织VEGF及微血管密度影响。方法:将45只Wistar大鼠分为正常对照组、模型对照组、姜黄素组各15只,正常对照组正常饲养,以间断小剂量二乙基亚硝胺溶液(DEN)诱发大鼠肝癌作为模型对照组,以在模型建立的同时接受姜黄素干预的大鼠作为姜黄素组。比较各组血清中低氧诱导因子-1α、血管内皮生长因子、肝功能指标以及微血管密度。结果:模型对照组以及姜黄素组血清中低氧诱导因子-1α、血管内皮生长因子、谷丙转氨酶以及谷草转氨酶均明显高于正常对照组(P<0.05);姜黄素组血清中上述指标明显低于模型对照组(P<0.05)。正常对照组肝组织血管内皮生长因子表达不明显,模型对照组肝组织血管内皮生长因子呈高表达,姜黄素组血管内皮生长因子表达降低(P<0.05)。模型对照组以及姜黄素组微血管密度明显高于正常对照组(P<0.05);姜黄素组微血管密度明显低于模型对照组(P<0.05)。结论:姜黄素可有效抑制原发性肝癌模型大鼠的血管生成,降低微血管密度,降低VEGF表达。
Objective: To observe the effect of curcumin on VEGF and microvessel density in primary liver cancer model rats. Methods: Forty-five Wistar rats were divided into normal control group, model control group and curcumin group. The normal control group was fed with intermittent low dose diethylnitrosamine solution (DEN) induced hepatocellular carcinoma The model control group was treated with curcumin while the model was established as a curcumin group. Hypoxia-inducible factor-1α, vascular endothelial growth factor, liver function index and microvessel density in each group were compared. Results: The serum levels of hypoxia inducible factor-1α, vascular endothelial growth factor, alanine aminotransferase and aspartate aminotransferase in the model control group and the curcumin group were significantly higher than those in the normal control group (P <0.05). The above indexes in the curcumin group were significantly higher than those in the control group Lower than the model control group (P <0.05). The expression of vascular endothelial growth factor (VEGF) in the liver of the model control group was higher than that in the normal control group, but decreased in the curcumin group (P <0.05). The microvessel density in model control group and curcumin group was significantly higher than that in normal control group (P <0.05). The microvessel density in curcumin group was significantly lower than that in model control group (P <0.05). Conclusion: Curcumin can effectively inhibit angiogenesis, reduce the density of microvessel and decrease the expression of VEGF in primary hepatocarcinoma model rats.