NF-κB对重症急性胰腺炎大鼠甲状旁腺激素受体表达和低钙血症的作用
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摘要
目的探讨核转录因子(NF-κB)对重症急性胰腺炎(SAP)大鼠甲状旁腺激素受体(PTHR1)表达的作用和对低钙血症的影响。
     方法将雄性SD大鼠72只随机分为3组,假手术组(SO)、SAP组、四氢化吡咯二硫代氨基甲酸脂(PDTC)预处理组(SAP+PDTC)各24只,以5%牛磺脱氧胆酸钠逆行胰胆管注射建立SAP模型,观察各组血清钙浓度以及胰腺病理改变,蛋白免疫印记技术(western blot)分析NF-κB表达量及甲状旁腺激素受体(PTHR1)表达量,逆转录-聚合酶链反应(RT-PCR)分析PTHR1 mRNA表达水平。
     结果SAP组制模后NF-κB在早期迅速活化,于3h达到高峰;骨组织PTHR1的表达6h后出现显著的下调;血清钙浓度6h后显著降低(p<0.05)。与SAP组比较,PDTC预处理组血清钙水平明显升高,PTHR1的表达上调(P<0.01),NF-κB的峰值降低。
     结论NF-κB可能通过对细胞因子的激活间接下调组织PTHR1的表达,致SAP血清钙显著下降。PDTC对改善SAP低钙血症有重要意义。
Objective To investigate the role of nuclear factor-kappa B(NF-κB) on the expression of parathyroid hormone receptor (PTHR1) and serum calcium level with severe acute pancreatitis (SAP) rats.
     Methods 72 male Sprague-Dawley rats were randomly divided into sham operation group (SO), SAP group, pyrrolidine dithiocarbamat (PDTC) pretreated SAP group (SAP+PDTC), 24 rats each group. SAP model was developed by injecting 5% sodium taurodeoxycholate into biliary-pancreatic duct. Serum calcium, the expression of NF-κB and PTHR1 by western blot and the expression of PTHR1 by RT-PCR were determined at 0.5, 1, 3, 6 hour after operations.
     Results NF-κB is activated soon after SAP and reaches the peak at 3 hour, then the expression of PTHR1 in bone and kidney down regulates. Serum levels of calcium is significantly reduced after 6 hour. As compared with SAP group, the level of NF-κB is decreased and the levels of PTHR1 and serum calcium are increased markedly in SAP+PDTC group.
     Conclusion NF-κB may down regulate the expression of PTHR1 in bone and kidney through complicated interreactions among many kinds of cytokines, leading to the hypocalcaemia of SAP.
引文
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