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Comparative effects of water immersion pretreatment on three different acute pancreatitis models in rats

机译:浸水预处理对三种大鼠急性胰腺炎模型的比较作用

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Cells respond to stress by upregulating the synthesis of cytoprotective heat shock proteins (HSPs) and antioxidant enzymes. The aim of this study was to compare the effects of cold (CWI) or hot water immersion (HWI) stress on three different acute pancreatitis models (cholecystokinin octapeptide (CCK), sodium taurocholate (TC), and L-arginine (Arg)). We examined the levels of pancreatic HSP60, HSP72, and antioxidants after the water immersion stress. Male Wistar rats were injected with CCK, TC, or Arg at the peak level of pancreatic HSP synthesis, as determined by Western blot analysis. HWI significantly elevated HSP72 expression and CWI significantly increased HSP60 expression in the pancreas. Water immersion stress decreased the levels of pancreatic antioxidants. CWI and HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. CWI pretreatment decreased pancreatic edema and the serum amylase level; however, the morphological damage was more severe in TC-induced acute pancreatitis. Overall, CWI and HWI pretreatment only decreased the serum cytokine concentrations in Arg-induced pancreatitis. CWI and HWI resulted in differential induction of pancreatic HSP60 and HSP72 and the depletion of antioxidants. The findings suggest the possible roles of HSP60 and (or) HSP72 (but not that of the antioxidant enzymes) in the protection against CCK- and TC-induced acute pancreatitis. Unexpectedly, CWI pretreatment was detrimental to the morphological parameters of TC-induced pancreatitis. It was demonstrated that CWI and HWI pretreatment only influenced cytokine synthesis in Arg-induced pancreatitis.
机译:细胞通过上调细胞保护性热休克蛋白(HSP)和抗氧化酶的合成来应对压力。这项研究的目的是比较冷(CWI)或热水浸泡(HWI)应激对三种不同的急性胰腺炎模型(胆囊收缩素八肽(CCK),牛磺胆酸钠(TC)和L-精氨酸(Arg))的影响。我们在浸水后检查了胰腺HSP60,HSP72和抗氧化剂的水平。通过蛋白质印迹分析确定,雄性Wistar大鼠在胰腺HSP合成的峰值水平处注射了CCK,TC或Arg。 HWI显着提高胰腺中HSP72表达,而CWI显着增加胰腺中HSP60表达。浸水压力降低了胰腺抗氧化剂的水平。 CWI和HWI预处理改善了CCK诱发的胰腺炎的大部分检查实验室和形态学参数。 CWI预处理可降低胰腺水肿和血清淀粉酶水平;然而,在TC诱发的急性胰腺炎中,形态损害更为严重。总体而言,CWI和HWI预处理只能降低Arg诱导的胰腺炎中血清细胞因子的浓度。 CWI和HWI导致胰腺HSP60和HSP72的差异诱导以及抗氧化剂的消耗。研究结果表明,HSP60和(或)HSP72(但不是抗氧化酶的作用)在预防CCK和TC诱发的急性胰腺炎中可能发挥作用。出乎意料的是,CWI预处理不利于TC诱发的胰腺炎的形态学参数。结果表明,CWI和HWI预处理仅影响Arg诱导的胰腺炎中细胞因子的合成。

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