Expression And Correlation Of HMGB1, RAGE And TNF-αin Placenta Of Gestational Diabetes Mellitus

Object:The purpose of this study was to investigate the expression and correlation of HMGB1、RAGE、TNF-a in gestational diabetes mellitus. we measured the level of HMGB1、RAGE、TNF-αprotein expression in placenta tissues obtained from the patient with gestational diabetes mellitus and normal pregnancy, to explore the difference and relationship between them and provide a new thinking way for clinical treatment and prevention.Method:A case-control study was performed in 30 women with gestational diabetes mellitus and 31 cases of normal 50g glucose challenge test(50g GCT)as control recruited from Jul 2011 to Tue 2012 in department of Obstetrics, the First Affiliated Hospital of Guangxi Medical University. All the samples were gotten from the maternal surface of the placenta after the labor immediately. To compare their clinical feature and the localized protein expression of HMGB1、RAGE、TNF-αin placenta of gestational diabetes mellitus and normal pregnancy by immunohistochemistry way.Result:(1) Women of two groups had expressed HMGB1、RAGE and TNF-a;(2)The localized protein expressions of HMGB1、RAGE and TNF-a were significantly higher in placenta of gestational diabetes mellitus than in control group (p<0.01,p<0.05 respectively). (3) There showed a significant linear positively correlation among HMGB1、RAGE and TNF-a in placenta of gestational diabetes mellitus (r=0.876,r=0.784,r=0.853, p<0.01)Conclusion:In the study we found that the increased expression of HMGB1、RAGE and TNF-a in placenta of gestational diabetes mellitus prompted the three may participate in the gestational diabetes mellitus patients of chronic inflammatory response,insulin resistance and islet cells damage and other pathophysiological processes, and TNF-a may regulate the expression of HMGB1 by stimulating macrophage activation; then HMGB1 by combinating with its receptor RAGE further activate monocyte-macrophage cells to release more TNF-α. Their interacted and collaborative function maintained and enlarged inflammatory, and thus participate in the pathophysiological process in gestational diabetes mellitus.