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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 effect of macrophage migration inhibitory factor antagonist (ISO-1) on endometriosis. Methods: The nude mice were used as the research object to establish the animal model of endometriosis. The macrophage migration inhibitory factor antagonist was used to intervene to observe the survival rate and weight change of endometriosis mice. -PCR was used to detect the expression of MMP-2, TIMP-2, VEGF and TNF-αmRNA. The expression of TNF-αprotein was detected by ELISA . Results: ISO-1 had no significant effect on the survival rate of endometriosis mice, but increased the body weight (P <0.05). ISO-1 reduced the expression of MMP-2, VEGF and TNF-α in the endometriosis-damaged mice (P <0.05), but had no effect on the expression of TIMP-2. CONCLUSIONS: Macrophage migration inhibitory factor is specifically blocked and can significantly inhibit the remodeling of damaged tissue, angiogenesis and inflammation, eventually affecting the tissue growth and further deterioration of endometriosis, which may be clinical treatment A new strategy of endometriosis.