The Expression Of TGF-β1、Smad3and IFN-γin The Endometrium And Fibrosis Tissue Of Patients With Intrauterine Adhesions And Its Clinical Meaning

Background and PurposeIntrauterine adhesions is caused by injuries or infections that induce intrauterine endometrium base layer damaged and irregenerative and intrauterine scar formation.These lead to the form of intrauterine abnormal which about90%is due to excessive curettage.In recent years,with the increase that the chance of uterine cavity operation and the development of modern hysteroscopy technology,its prevalence rate is increasing year by year,it seriously affected the modern women’s quality of life and fertility requirements. So far the exact pathogenesis of Intrauterine adhesions is uncertain.It may be related to the abnormal expression of some cytokines promoting wound repair or inhibition of tissue fibrosis.Therefor,it is an important theoretical basis that to discuss the expression of TGF-β1、Smad3and IFN-γ in the fibrosis tissue and endomertrium near the fibrosis of patients with intrauterine adhesions,for the pathogenesis of Intrauterine adhesions,prevent the formation of IUA and postoperative recurrence and use of TGF-beta antibodies and TGF-beta1inhibitor anti fibrosis treatmentNow,TGF-β1is recognized as the strongest fibrosis factors,and it is the key mediating factor of fibrous scar formation pathways. TGF-β1as a kind of multifunctional cytokine induce tissue fibrosis, through interaction associated with some inflammatory cytokines, fibroblast proliferation in great quantities, excessive extracellular matrix deposition.Moreover, TGF-beta1through to chemotaxis migration of the vascular endothelial cell and entrainment of small tube skin growth factor (VEGF), promote blood vessels of the formation of scar tissue.Smads proteins family including Smad1～10.Smad3protein is an important signal transduction molecule which transduces the signal originated from combination of TGF-beta activated and receptors from cytoplasmic to nuclei.Through the TGF-beta1/Smad3pathways to increase collagen synthesis and deposition of extracellular matrix, tissue fibrous scar formation.It is the more cleat that IFN-gamma is the adjustment factor of restrain tissue fibrosis,It has a variety of biological functions,such as influence cell growth and differentiation,and immune regulation.Causes of TGF-beta1/Smad3pathway of signal in transmission process is blocked, inhibited TGF-beta1and Smad3protein expression,and reduce the deposition of extracellular matrix.Material and Methods1.GroupingThe experimental group:Take the fibrosis tissue and endomertrium near the fibrosis tissue in30patients dignosed as intrauterine adheious in department of gynaecology and obstetrics of the second affiliated hospital of Zhengzhou University from May2012to October2012.The control group:Take normal endometrium in30infertility patients who were accepted hysteroscopic examination in depart tment of gynaecology and obstetrics of the second affiliated hospital of Zhengzhou University from May2012to October2012.Take normal intima proved by pathology.2.MethodsUse Immunohistohistochemistry SP method to detect the expression of TGF-beta1, Smad3and IFN-γ in three tissue.3.Statistical analysisUsing SPSS package for windows17.0statistical analysis to test all data.The expression of TGF-beta1, Smad3and IFN-y in three tissue is compared by Oneway ANOVA;Different binary comparison between the groups uses the LSD-t test.The correlation between groups is tested by Pearson correlation analysis.The level for significance tests is0.05.Results1. Expression of TGF-beta1(1)The expression of TGF-betal in the fibrosis tissue is higher than that in endometrium near the fibrosis tissue.The difference is significant statistically (P<0.05).(2)The expression of TGF-beta1in the fibrosis tissue is higher than that in normal endometrium tissue.The difference is significant statistically(P<0.05).(3)The expression of TGF-beta1in endometrium near the fibrosis tissue is higher than that in normal endometrium tissue.The difference is significant statistically(P<0.05).2.Expression of Smad3(1)The expression of Smad3in the fibrosis tissue is higher than that in endometrium near the fibrosis tissue.The difference is significant statistically (P<0.05).(2)The expression of Smad3in the fibrosis tissue is higher than that in normal endometrium tissue.The difference is significant statistically(P<0.05).(3)The expression of Smad3in endometrium near the fibrosis tissue is higher than that in normal endometrium tissue.The difference is significant statistically (P<0.05).3.Expression of IFN-γ(1)The expression of IFN-γ in the fibrosis tissue is lower than that in endometrium near the fibrosis tissue.The difference is significant statistically (P<0.05).(2)The expression of IFN-γ in the fibrosis tissue is lower than that in normal endometrium tissue.The difference is significant statistically(P<0.05).(3)The expression of IFN-γ in endometrium near the fibrosis tissue is lower than that in normal endometrium tissue.The difference is significant statistically(P<0.05).4.Relationship between TGF-beta1and Smad3 There is a positive correlation between the expression of TGF-betal and the expression of Smad3in the fibrosis tissue and in endometrium near the fibrosis tissue.5.Relationship between TGF-betal and IFN-γThere is a negative correlation between the expression of TGF-betal and the expression of IFN-γ in the fibrosis tissue and in endometrium near the fibrosis tissue.Conclusions1.TGF-betal and Smad3are higher expressions in the fibrosis tissue and in endometrium near the fibrosis tissue,which related to the formation of Intrauterine adhesions.2.IFN-γ is lower expression in the fibrosis tissue and in endometrium near the fibrosis tissue.There is a negative correlation between the expression of TGF-betal and the expression of IFN-γ, which related to the formation of Intrauterine adhesions.3.Through the relationship of TGF-beta1, Smad3and IFN-γ in TGF-beta1/Smad3pathways, the anti fibrosis treatment is likely to be used in the treatment of uterine cavity adhesion.