人参皂苷Rg3不同给药途径对大鼠子宫内膜异位症血管生成抑制作用的比较

目的观察不同给药途径人参皂苷Rg3对大鼠子宫内膜异位症(EMs)异位囊肿体积、组织中血管内皮生长因子(VEGF)、微血管密度(MVD)的影响和抗血管生成作用。方法参照Jones方法建立Wistar大鼠EMs动物模型,3周后将建模成功的大鼠随机分为经口服灌胃和腹腔注射给药2、4、6及8周组共8组,观察两种给药途径对大鼠EMs异位囊肿的体积抑制率、组织中的VEGF和MVD的表达。结果①两种不同给药途径随着给药时间的延长大鼠EMs异位囊肿体积抑制率逐渐增加、组织中MVD和VEGF表达逐渐减少;②Rg3腹腔给药起效快,治疗2、4、6周时较口服灌胃体积抑制率显著增加(P<0.05),但治疗8周后,口服效果迅速增加,两组体积抑制率差异无统计学意义(P>0.05);③口服给药8周后体积抑制作用最明显,MVD和VEGF表达最少(P>0.05)。结论Rg3对大鼠EMs异位囊肿体积、组织中MVD和VEGF表达及新生血管生成均有明显抑制作用。经腹腔给药途径作用快。

Inhibition of angiogenesis in endometriotic mice by Ginsenosides Rg3 administered through varied routes

Objective To investigate the impacts of Ginsenosides Rg3 administered through varied routes on volume of endometriotic cyst, tissue level of vascular endothelial growth factor (VEGF), microvessel density (MVD) and angiogenesis in endometriosis (EMs) rat models. Methods Endometriosis models were established using Wistar rats as described by Jones. Three weeks later, validated models were randomized into eight groups receiving Rg3 by oral gavage or intraperitoneal injection for 2, 4, 6 and 8 weeks, respectively. The volume inhibition rate of ectopic EMs cysts, tissue MVD and expression of VEGF were measured in rats treated through the two different routes. Results ①Over time, the volume inhibition rate of ectopic EMs cysts increased, while tissue MVD and expression of VEGF gradually declined with both routes of medication; ②Intraperitoneal administration of Rg3 appeared to be fast-acting, with significantly greater inhibition of EMs cyst volume compared with oral gavage at 2, 4 and 6 weeks (P<0.05); however, at 8 weeks, the rapidly growing effects by oral gavage led to no significant difference in the volume of cysts between two groups (P>0.05); ③The greatest inhibition of cyst volume and lowest MVD and VEGF expression were seen at 8 weeks (P<0.05). Conclusion Ginsenoside Rg3 may significantly inhibit the volume of EMs cyst, tissue VEGF, MVD and angiogenesis in endometriotic rat models. Such effects appeared earlier with Rg3 administered intraperitoneally.