人参皂苷Rg1与Rb1在心肌缺血复合肿瘤病理环境下的作用研究

目的:观察三七总皂苷主要成分人参皂苷Rg1和Rb1在心肌缺血复合肿瘤病理环境下的作用,并通过研究血管新生探索其可能的作用机制。方法:采用小鼠经皮下移植LLCs肿瘤细胞及腹腔注射异丙肾上腺素的方法制备肿瘤复合心肌缺血动物模型,再随机分为模型组、人参皂苷Rg1组、人参皂苷Rb1组;另设正常对照组。Rg1组和Rb1组分别予腹腔注射Rg1、Rb1(50 mg/kg);正常组与模型组给予等体积生理盐水。连续干预15 d后,比较各组小鼠的肿瘤生长情况、心肌组织病理形态学变化及通过免疫组织化学的方法检测心肌和肿瘤组织中CD34、vWF的蛋白表达。结果:人参皂苷Rg1及Rb1治疗组小鼠移植肿瘤生长显著受到抑制,其平均瘤重显著低于模型组(P0.05);两组心肌组织缺血损伤显著改善,胶原含量明显减少(P0.05,P0.01);同时心肌组织中CD34和vWF蛋白表达量显著升高,而肿瘤组织中CD34和vWF蛋白表达量显著降低,与模型组比较差异有统计学意义(P0.05,P0.01)。结论:三七总皂苷主要活性成分人参皂苷Rg1和Rb1在心肌缺血复合肿瘤病理环境下显著抑制LLCs肿瘤生长,并显著改善心肌缺血损伤,其双向作用的机制可能与对血管生成双向调节作用有关。

Effects of Ginsenosides Rg1 and Rb1 in Myocardial Ischemia Complex Pathological Environment of Neoplasia

Objective： To investigate the effects of ginsenosides Rg1 and Rb1 in myocardial ischemia complex pathological environment of neoplasia and to explore its mechanism by studying the angiogenesis. Methods： The mice models were established by subcutaneously transplanting LLCs tumor cells and intraperitoneally injecting isoproterenol,and then randomly divided into the model group,ginsenosides Rg1 group and ginsenosides Rb1 group; a normal control group was set up also. The ginsenosides Rg1 group and ginsenosides Rb1 group were treated by ginsenosides Rg1 and ginsenosides Rb1 respectively（50 mg/kg）; the normal group and the model group were treated with the same volume of normal saline. After intervened for15 days continuously,we compared the tumor growth,pathomorphological changes of cardiac muscle tissues in rats among the groups and detected the expressions of CD34 and vWF in myocardium and tumor tissues by immunohistochemical technology.Results： The tumor growth was significantly inhibited in the ginsenosides Rg1 group and the ginsenosides Rb1 group,the average tumor weight of the two groups was significantly less than that of the model group（ P〈0. 05）; the damage of myocardial ischemia of the ginsenosides Rg1 and Rb1 groups was significantly improved,and the collagen was decreased markedly（ P〈0. 05,P〈0. 01）; expressions of CD34 and vWF were significantly up-regulated in myocardium tissues but down-regulated in tumor tissues of the ginsenosides Rg1 and Rb1 groups,with a significant difference between the two groups and the model one（ P〈0. 05,P〈0. 01）. Conclusion： Ginsenosides Rg1 and ginsenosides Rb1,the primary reactive compositions of PNS can inhibit the LLCs tumor growth and improve the myocardial ischemia injury significantly in the myocardial ischemia and tumor complex pathological environment,suggesting that its bidirectional mechanism may be correlated with the bidirectional regulation of angiogenesis.