摘要
目的:探讨巨噬细胞迁移抑制因子拮抗剂(ISO-1)对子宫内膜异位症的影响。方法:以裸鼠为研究对象,构建子宫内膜异位元症动物模型,应用巨噬细胞迁移抑制因子拮抗剂进行干预,观察子宫内膜异位症小鼠的成活率和体重变化;采用RT-PCR检测基质金属蛋白酶-2(MMP-2),基质金属蛋白酶抑制剂-2(TIMP-2),血管内皮细胞生长因子(VEGF),TNF-αmRNA的表达,ELISA检测TNF-α蛋白的表达。结果:ISO-1对子宫内膜异位症小鼠的存活率无明显影响,但可增加其体重(P<0.05)。ISO-1减少子宫内膜异位症小鼠受损组织中MMP-2、VEGF、TNF-α的表达(P<0.05),但对TIMP-2的表达无明显影响。结论:巨噬细胞迁移抑制因子被特异性阻断后,可明显抑制受损组织的重构、血管生成和炎症,最终影响子宫内膜异位症的组织生长及进一步恶化,这可能是临床治疗子宫内膜异位症的新策略。
Objective： To investigate the macrophage migration inhibitory factor antagonist （ISO- 1）on the endometriosis. Methods： Endometrial heterotopic disease mice models were build, and treated with macrophage cell migration inhibition factor antagonists to intervene, the mice survival and weight were observed. Matrix metalloproteinase-2 （MMP-2）-2, matrix rnetalloproteinase inhibitors （TIMP-2）, vascular endothelial growth factor （VEGF） and TNF-αlpha mRNA expressions were detected by RT-PCR, ELISA was used to detect the TNF-α protein expression. Results： There were no significant effect on survival rate after ISO-1 intervene, but the body weight improved （P〈0.05）, and expressions ofMMP-2, ofVEGF, TNF-α reduced in endometrial endometriosis mice （P 〈0.05）, the expression of TIMP-2 were not changed. Conclusion： The macrophage migration inhibitory factor was specific inhibitor, may significantly inhibit the reconstruction of, damaged tissue, angiogenesis and inflammation, and ultimately affect tissue growth and further deterioration of endometriosis, which may be of clinical treatment of uterine endometriosis of the new strategy.
出处
《现代生物医学进展》
CAS
2013年第2期253-256,268,共5页
Progress in Modern Biomedicine
基金
湖南省教育厅基金项目(09C632)
