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首页> 外文期刊>Life sciences >Effects of pantoprazole in experimental acute pancreatitis.
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Effects of pantoprazole in experimental acute pancreatitis.

机译：top托拉唑在实验性急性胰腺炎中的作用。

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AIMS: Oxidative stress with free radicals plays a crucial role in acute pancreatitis (AP). Pantoprazole (PPZ), widely used as a proton pump inhibitor, possesses reactivity towards hydroxyl radicals. The aim of the study was to examine the effect of PPZ on the course of experimental AP. MAIN METHODS: Mild AP was induced in rats by caerulein (n=12). Severe AP was induced by infusion of glycodeoxycholic acid (10mM) into the pancreatic duct combined with caerulein (n=12). Both AP models were randomized to PPZ treatment (20mg/kg at baseline and after 12h) or placebo. Control animals received Ringer solution (n=6) without AP induction. After 24h severity of AP was examined by histology, enzyme levels, edema and inflammatory markers (myeloperoxidase, protein profiling). Furthermore, CD62P and CD31 for leukocyte and platelet activation were investigated. KEY FINDINGS: Histology showed that PPZ treatment reduced tissue infiltration of inflammatory cells and acinar cell necrosis in severe AP. After PPZ treatment CD62P expression in mild AP and CD31 expression in severe pancreatitis decreased, indicating an inhibition of platelet activation. In mild and severe AP, PPZ significantly decreased amylase, LDH, edema and myeloperoxidase activity. Protein profile of pancreatic juice and serum revealed different spectra and less pancreatic juice proteins in PPZ treated groups indicating less acinar cell leakage. SIGNIFICANCE: PPZ possesses anti-inflammatory in vivo properties and attenuates the course of AP. This is mediated via a reduced expression of inflammatory and adhesive proteins with a consecutive decrease in platelet and leukocyte activation as key steps in the pathogenesis of AP.
机译：目的：具有自由基的氧化应激在急性胰腺炎（AP）中起着至关重要的作用。 top托拉唑（PPZ），广泛用作质子泵抑制剂，对羟基具有反应活性。这项研究的目的是检查PPZ对实验性AP的影响。主要方法：轻柔霉素诱导大鼠轻度AP（n = 12）。通过将胰岛脱氧胆酸（10mM）与青霉素（n = 12）联合输注到胰管中来诱导严重AP。两种AP模型均随机接受PPZ治疗（基线时和12h后为20mg / kg）或安慰剂。对照动物接受无AP诱导的林格溶液（n ＝ 6）。 24小时后，通过组织学，酶水平，水肿和炎性标志物（髓过氧化物酶，蛋白质谱）检查AP的严重程度。此外，研究了用于白细胞和血小板活化的CD62P和CD31。主要发现：组织学显示，PPZ治疗可减轻严重AP患者炎性细胞的组织浸润和腺泡细胞坏死。 PPZ处理后，轻度AP中的CD62P表达和重症胰腺炎中的CD31表达下降，表明血小板活化受到抑制。在轻度和重度AP中，PPZ显着降低淀粉酶，LDH，水肿和髓过氧化物酶活性。胰液和血清的蛋白谱显示不同的光谱，PPZ处理组的胰液蛋白较少，表明腺泡细胞渗漏较少。意义：PPZ具有抗炎的体内特性，可减轻AP的病程。这是通过炎症和粘附蛋白表达的降低，以及血小板和白细胞激活的连续降低（作为AP发病机理的关键步骤）来介导的。

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