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Rosiglitazone, a peroxisome proliferator-activated receptor gamma (PPARgamma)-specific agonist, as a modulator in experimental acute pancreatitis

机译:罗格列酮,一种过氧化物酶体增殖物激活的受体γ(PPARgamma)特异性激动剂,作为实验性急性胰腺炎的调节剂

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Background The purpose of this experiment was to investigate the role of PPAR ligands in the course of inflammation and of rosiglitazone, a PPAR-gamma-specific agonist, on the course of experimental acute pancreatitis (EAP). Material and Method EAP was induced by administration of 5% sodium taurocholate injected into the pancreatic duct. The inflammatory activity was evaluated by biochemical scores (alpha-amylase, lipase, aminotransferases, and bilirubin), morphological changes (determined by light microscopy, H+E stained), and immunohistochemical reactions (ICAM, nitrotyrosine). Results Rosilgitazone administered in the course of EAP at a dose 50 mg/kg p.o. decreased the intensity of morphological changes (edema, inflammatory infiltrates, necrosis, and erythrocyte extravasations). In the rosiglitazone-treated animals all the biochemical parameters of EAP were statistically significantly decreased. Immunohistochemical reactions against ICAM-1 and nitrotyrosine showed that rosiglitazone decreased the intensity of inflammatory reactions in the groups of treated animals. Conclusions PPAR-gamma agonists modulate the course of the inflammatory reaction. The administration of rosiglitazone decreased the intensity of the inflammatory process in the course of sodium taurocholate-induced EAP.
机译:背景本实验的目的是研究PPAR配体在炎症过程中的作用以及罗格列酮(PPAR-γ特异性激动剂)在实验性急性胰腺炎(EAP)的过程中的作用。材料和方法EAP是通过向胰管中注射5%牛磺胆酸钠来诱导的。通过生化评分(α-淀粉酶,脂肪酶,氨基转移酶和胆红素),形态变化(通过光学显微镜,H + E染色确定)和免疫组化反应(ICAM,硝基酪氨酸)评估炎症活性。结果罗格列酮在EAP过程中以50 mg / kg p.o的剂量给药。降低了形态变化的强度(水肿,炎性浸润,坏死和红细胞外渗)。在罗格列酮治疗的动物中,EAP的所有生化参数均在统计学上显着降低。针对ICAM-1和硝基酪氨酸的免疫组织化学反应表明,罗格列酮降低了治疗组动物的炎症反应强度。结论PPAR-γ激动剂可调节炎症反应的进程。罗格列酮的施用降低了牛磺胆酸钠诱导的EAP过程中炎症过程的强度。

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