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作 者:王莉莉[1] 孙磊[1] 郝蕊[1] 朱梓炎[1] 叶德全[1]
出 处:《现代生物医学进展》2017年第13期2574-2577,2573,共5页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(31470865;81202316)
摘 要:普遍认为,急性胰腺炎起始于腺泡细胞内的胰蛋白酶原激活,随后引起的炎症反应加剧病情,也是多器官功能衰竭的主要原因。然而,最新的研究表明,急性胰腺炎引起的炎症反应是不依赖于胰蛋白酶原激活的独立病理过程。趋化因子作为能引起细胞趋化的细胞因子,通过与趋化因子受体作用,不但能调控淋巴细胞的生长、成熟和迁移,也参与多种炎症疾病与癌症的病理过程。近年来,多项研究已经阐述趋化因子及趋化因子受体在急性胰腺炎的发病发展过程中起到至关重要的作用。本文总结了CC,CXC和CX3C趋化因子家族成员在参与急性胰腺炎的炎症反应及对胰腺损伤的修复的研究进展,这将为AP临床治疗方案的设计提供新思路。It is generally believed acute pancreatitis (AP) is initiated from pathologic trypsinogen activation in pancreatic acinar cells,and the subsequent inflammation response exacerbates the illness,which will result in multiple-organ dysfunction.However,a recent research clarified that the inflammation response in AP is independent from pathologic trypsinogen activation.Chemokines,belong to cytokines family,interact with their receptors to cause chemotaxis,they are not only involved in the growth,maturation and migration of lymphocytes,but also play a role in the pathogenesis of many inflammatory diseases and cancer.Recent years,various researches have been clarified the important role of chemokines and chemokine receptors in the pathogenesis of AP.In this review,the involvement of CC,CXC and CX3C chemokine family members in the inflammatory response in AP and in the repair of injured pancreas in AP are summarized.This may provide a new idea in the design for clinical treatment of AP.
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