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The effects of hypo- and hyperthermic pretreatment on sodium taurocholate-induced acute pancreatitis in rats.

机译:低温和高温预处理对牛磺胆酸钠引起的大鼠急性胰腺炎的影响。

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INTRODUCTION: Heat shock proteins (HSPs) have indispensable functions in the synthesis, degradation, folding, transport, and translocation of intracellular proteins. HSPs are proteins that help cells to survive stress conditions by repairing damaged proteins. AIM: To investigate the potential effects of HSP preinduction by cold-water (CWI) or hot-water immersion (HWI) on sodium taurocholate (TC)-induced acute pancreatitis in rats. METHODOLOGY: TC was injected into the common biliopancreatic duct of the animals at the peak level of HSP synthesis, as determined by Western blot analysis. The rats were killed by exsanguination through the abdominal aorta 6 hours after the TC injection. The serum amylase activity, the IL-1, IL-6 and TNF-alpha levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase, and trypsinogen were measured, and a biopsy for histology was taken. RESULTS: HWI significantly elevated HSP72 expression, whereas CWI significantly increased HSP60 expression. It was demonstrated that CWI pretreatment ameliorated the pancreatic edema and the serum amylase level increase, whereas the morphologic damage was more severe in this form of acute pancreatitis. HWI pretreatment did not have any effects on the measured parameters in TC-induced pancreatitis. CONCLUSIONS: The findings suggest a possible role of HSP60, but not HSP72, in the slight protection in the early phase of this necrohemorrhagic pancreatitis model.
机译:简介:热激蛋白(HSP)在细胞内蛋白的合成,降解,折叠,转运和易位中具有不可或缺的功能。 HSP是通过修复受损的蛋白质来帮助细胞在压力条件下生存的蛋白质。目的:研究冷水(CWI)或热水浸泡(HWI)预诱导HSP对牛磺胆酸钠(TC)诱导的大鼠急性胰腺炎的潜在影响。方法学:通过蛋白质印迹分析确定,在HSP合成的峰值水平,将TC注入动物的胆总管。 TC注射6小时后,通过腹主动脉放血杀死大鼠。测量血清淀粉酶活性,IL-1,IL-6和TNF-α水平,胰腺重量/体重比以及DNA,蛋白质,淀粉酶,脂肪酶和胰蛋白酶原的胰腺含量,并进行组织活检被拿走。结果:HWI显着提高了HSP72的表达,而CWI显着提高了HSP60的表达。事实证明,CWI预处理可减轻胰腺水肿和血清淀粉酶水平升高,而在这种形式的急性胰腺炎中,形态损害更为严重。 HWI预处理对TC诱发的胰腺炎中的测量参数没有任何影响。结论:研究结果提示,在这种坏死性出血性胰腺炎模型的早期阶段,HSP60(而非HSP72)可能在轻微的保护中可能发挥作用。

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