Objective:To detect the normal glucose tolerance, impaired glucose pregnancyinflammatory factors of pregnant women and pregnant women withgestational diabetes mellitus maternal and fetal side decent tolerance(tumor necrosis factor alpha and interleukin-6) and adipocytokines(leptin and adiponectin) changes in protein positive expression intensityand protein levels, discussion on the important role of inflammatorycytokines and adipokines play in the pathogenesis of gestational diabetesmellitus and its clinical significance in.Methods:Collected in our hospital from2013June to2014August productionof100pregnant women, divided into normal glucose tolerance pregnancygroup (NGT group),24patients with impaired glucose tolerance group(IGT group) and31cases of gestational diabetes mellitus group (GDMgroup)45cases. Three groups of pregnant women were collectedimmediately after delivery fetal side of the placenta and maternal side, apart of cryopreservation, part of a fixed in4%paraformaldehyde solution.Using immunohistochemical method of tumor necrosis factor alpha in three groups were detected fetal side of placenta and maternal side (TNF-alpha), interleukin-6(IL-6), protein positive expression of leptin andadiponectin. Using enzyme-linked immunosorbent method (ELISAmethod) to detect tumor group three fetal side of placenta and maternalside necrosis factor alpha (TNF-alpha), interleukin-6(IL-6), leptin andadiponectin protein content level.Results:1.Groups of placental inflammatory factor (TNF-α and IL-6)comparison of expression positive strengthCompared with group A, group B, group C of fetal side and the maternalside of TNF-alpha, IL-6protein positive expression were increased inintensity and C group than in B group, the difference was significant(P<0.01); the maternal side TNF-α, IL-6of the two groups weresignificantly higher than that of fetal side expression was statisticallysignificant (P<0.01).2. Groups of placental adipokines (leptin and adiponectin)comparison of expression positive strength.Compared with group A, were higher in C group than in B group and Bgroup, the expression of leptin protein positive strength, GDM group offetal side and the maternal side, adiponectin protein expression levelswere decreased and the C group was lower than that of B group, thesignificant difference with statistical significance (P<0.01); the expression of matrix side leptin two group were significantly higher thanthat of fetal side (P<0.01), the expression of adiponectin is lower than thatof the maternal side fetal side with statistical significance (P<0.05).3. Groups of placental inflammatory factor (TNF-α and IL-6)protein content results Compared with A group, B group, C group of fetalside and the maternal side protein IL-6content in TNF-alpha, wereelevated and C group than in B group, the significant difference wasstatistically significant (P<0.01); the expression of TNF-alpha, IL-6matrix side the two groups were significantly higher than that of fetal sidewith statistical significance (P<0.01).4. Groups of placental adipokines (leptin and adiponectin) proteincontent results Compared with A group, B group, C group of fetal sideand the maternal side leptin protein content increased and the C groupthan in B group, adiponectin protein content decreased and the C groupwas lower than that of B group, the significant difference was statisticallysignificant (P<0.01); maternal leptin expression side two group weresignificantly higher than that of fetal side (P<0.01), the expression ofadiponectin is lower than that of the maternal side fetal side withstatistical significance (P<0.05).Conclusion:1.Gestational diabetes mellitus may upregulate the expression ofTNF-α, IL-6, leptin and adiponectin expression down regulated, and two groups of maternal side TNF-alpha, IL-6, leptin levels were significantlyhigher than that of fetal side, adiponectin expression below the fetal side.2. The upregulation of the expression of TNF-α, IL-6, leptin andadiponectin expression down regulated, may participate in the occurrenceof GDM, the process of development, play an important role in thepathogenesis of GDM. |