三七提取物对三硝基苯磺酸诱导溃疡性结肠炎大鼠结肠血管生成的研究

[目的]从血管生成角度研究三七提取物促进结肠溃疡愈合的作用机制。[方法]制备三硝基苯磺酸（TNBS）诱导溃疡性结肠炎（UC）大鼠，分为三七提取物低、中、高剂量组，柳氮磺胺吡啶（SASP）组，模型对照组，模型组和正常对照（正常）组。其中模型组于造模3d时处死，其余6组均在给药处理7d（即造模10d）时处死。取大鼠结肠病变部位标本，进行组织学评价；运用免疫组化染色法检测血管内皮生长因子（VEGF）、fms样酪氨酸激酶受体（FLT-1）和含有激酶插入区域的受体（KDR）、低氧诱导因子（HIF-1）蛋白表达；用RT-PCR法检测VEGF、FLT-1和KDR、HIF-1的mRNA表达。[结果]与模型对照组和SASP组比较，三七提取物低、中和高剂量组大鼠结肠黏膜炎症明显消除和溃疡愈合，杯状细胞数量及黏液增加，VEGF、FLT-1和KDR、HIF-1表达显著增加。[结论]血管生成在TNBS诱导大鼠UC形成和愈合过程中起重要作用。用药后VEGF、KDR、FLT-1和HIF-1表达增加。三七提取物通过上调VEGF、KDR、FLT-1和HIF-1表达促进血管生成，是其治疗UC的主要作用机制之一。

Research of panax notoginseng extractive on angiogenesis of ulcerative colitis in rats induced by trinitrobenzene sulfonic acid

[Objeetive]To study the role of angiogenesis in the formation and healing process of colitis in rats induced by trinitrobenzene sulfonie acid （TNBS）, and the possible regulating effect of panax notoginseng extractive （PNE）. [Methods]Rat colitis model was induced by TNBS. Rats were divided into PNE low dose group, PNE middle dose group, PNE high dose group, saliey- lazosulfapyridine （SASP） group, model group, model control group and normal control group. Rats of model group were sacrificed at 3 days , the other group rats were sacrificed after 7 days treatment. Histopathologieal assessment in the colonic mueosa, and detection of vascular endothelial growth factor （VEGF）, FLT1, KDR and hypoxia inducible factor 1（HIF1） protein expression by immunohistoehemistry staining were analyzed. VEGF, FLT1, KDR and HIF1 mRNA expression was analyzed by RT-PCR method. [Results] After 7 days treatment, the better colonic mueosal ulcer healing, higher increase of the number of goblet cells and mucus content, increase of cell proliferation at the ulcer margin, and markedly up-regulating expression of VEGF, FLT1, KDR and HIF1 were observed in the rats of PNE low, middle and high dose groups compared with model control group and SASP group. [Conclusion]Angiogenesis plays an important role in the formation and healing process of rat colitis induced by TNBS. PNE is able to enhance angiogenesis by up-regulating VEGF,KDR,Fltl and HIF1 expressions, which is the ma- jor mechanism of action in the treatment of ulcerative colitis.