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Interactions Between Neutrophils and Platelets in the Progression of Acute Pancreatitis

机译:中性粒细胞和血小板之间的相互作用在急性胰腺炎进展中

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Objective Severe acute pancreatitis is a serious disease, but its detailed mechanism has not yet been elucidated. We aimed to clarify the interaction between neutrophils and platelets in the pathogenesis of acute pancreatitis. Methods We induced acute pancreatitis in rats by injection of sodium taurocholate into the biliopancreatic duct and killed them over time. We observed the histological changes in pancreatic tissue with special attention to the dynamics of neutrophils and platelets. We also measured the concentrations of neutrophil- and platelet-derived factors in pancreatic tissue and blood samples. Results Neutrophils and platelets in the pancreatic tissue showed a similar pattern of migration. They initially spread in the interlobular connective tissue and finally into the lobules. The concentration of myeloperoxidase gradually increased in the inflamed pancreas until 24 hours and the concentration of thromboxane B2, plasminogen activator inhibitor 1, and CD41 also increased with time. Finally, the concentration of serum myeloperoxidase, citrullinated histone H3, and high-mobility group box 1 increased over time. Conclusions The interaction between neutrophils and platelets in pancreatic tissue plays an important role in the mechanism of advancing severity in acute pancreatitis. Circulating damage-associated molecular patterns induced by excessive local inflammation may lead to other organ injuries.
机译:客观严重的急性胰腺炎是一种严重的疾病,但其详细的机制尚未阐明。我们旨在阐明中性粒细胞和血小板之间的相互作用在急性胰腺炎的发病机制中。方法通过将牛磺酸钠注射到双偶极锰管中,诱导大鼠急性胰腺炎,随着时间的推移杀死它们。我们观察到胰腺组织的组织学变化,特别注意中性粒细胞和血小板的动态。我们还测量了胰腺组织和血液样品中的中性粒细胞和血小板衍生因子的浓度。结果胰腺组织中的中性粒细胞和血小板显示出类似的迁移模式。它们最初在角间结缔组织中铺展并最终进入小叶。髓氧化酶的浓度在发炎胰腺中逐渐增加,直至24小时,血液素活化剂抑制剂1和CD41的浓度随时间增加。最后,随着时间的推移,血清髓过氧化物酶,柑橘酰胺组蛋白H3和高迁移率组箱1的浓度增加。结论胰腺组织中嗜中性粒细胞和血小板之间的相互作用在推进急性胰腺炎的严重程度的机制中起着重要作用。通过过量局部炎症诱导的循环损伤相关分子模式可能导致其他器官损伤。

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