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目的:探讨磷酸化c-jun氨基末端激酶(p-JNK)蛋白在妊娠期糖尿病孕鼠子宫组织中的表达情况,及其在GDM发病机制中的作用。方法:用免疫组化和Western-blotting法检测妊娠期糖尿病大鼠(GDM组,n=10只)、给予JNK抑制剂SP600125(SP组,n=10只)和正常妊娠大鼠(正常妊娠组,n=10只)子宫组织中p-JNK的表达,同时检测空腹血糖水平(FPG)、空腹胰岛素水平(FINS)和胰岛素抵抗指数(HOMA-IR)。结果:①GDM组孕鼠FPG、FINS及HOMA-IR水平均明显高于正常妊娠组(P<0.05)。②p-JNK主要在子宫腺上皮、间质细胞和少量平滑肌细胞的胞浆和胞核中表达,GDM组子宫组织中p-JNK的表达水平明显高于正常妊娠组,差异有统计学意义(P<0.05)。JNK抑制剂SP600125干预后GDM孕鼠子宫组织中p-JNK表达显著减少(P<0.05)。③GDM组子宫组织中p-JNK蛋白表达水平与HOMA-IR呈正相关(r=0.763,P<0.05);SP组及正常妊娠组则均无相关性(r=0.549、0.482,P<0.05)。结论:JNK蛋白的活化与GDM胰岛素抵抗密切相关,p-JNK表达异常可能在GDM发病机制中发挥着重要的作用。
Objective: To investigate the expression of phosphorylated c-jun amino-terminal kinase (p-JNK) in uterus of pregnant mice with gestational diabetes mellitus and its role in the pathogenesis of GDM. Methods: The gestational diabetes mellitus (n = 10) and gestational diabetes mellitus (n = 10) were detected by immunohistochemistry and Western-blotting method. JNK inhibitor SP600125 (SP group, n = 10) and normal pregnant rats , n = 10). The expression of p-JNK in uterine tissue was also measured. Fasting plasma glucose (FPG), fasting insulin (FINS) and insulin resistance index (HOMA-IR) were also detected. Results: ①The levels of FPG, FINS and HOMA-IR in GDM group were significantly higher than those in normal pregnancy group (P <0.05). ②p-JNK was mainly expressed in the cytoplasm and nucleus of uterine glandular epithelium, stromal cells and a few of smooth muscle cells. The expression of p-JNK in uterine tissue of GDM group was significantly higher than that of normal pregnancy group (P <0.05). The expression of p-JNK in uterus of GDM pregnant mice significantly decreased after JNK inhibitor SP600125 intervention (P <0.05). ③The expression of p-JNK in uterine tissue of GDM group was positively correlated with HOMA-IR (r = 0.763, P <0.05). No correlation was found between SP group and normal pregnancy group (r = 0.549,0.482, P <0.05). Conclusion: The activation of JNK protein is closely related to insulin resistance in GDM. The abnormal expression of p-JNK may play an important role in the pathogenesis of GDM.