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本文引用的文献

1
Influence of nuclear factor kappaB activation on inflammatory mediators of alveolar macrophages in rats with acute necrotizing pancreatitis.核因子κB激活对急性坏死性胰腺炎大鼠肺泡巨噬细胞炎症介质的影响。
J Investig Med. 2010 Jan;58(1):38-42. doi: 10.2310/JIM.0b013e3181b91bd6.
2
In vitro, but not in vivo, reversibility of peritoneal macrophages activation during experimental acute pancreatitis.在实验性急性胰腺炎期间,腹膜巨噬细胞激活的可逆性仅在体外而非体内存在。
BMC Immunol. 2009 Jul 31;10:42. doi: 10.1186/1471-2172-10-42.
3
Leukocyte-endothelial interactions in inflammation.炎症中的白细胞-内皮细胞相互作用
J Cell Mol Med. 2009 Jul;13(7):1211-20. doi: 10.1111/j.1582-4934.2009.00811.x. Epub 2009 Jun 16.
4
Different cell death modes of pancreatic acinar cells on macrophage activation in rats.大鼠巨噬细胞激活后胰腺腺泡细胞的不同细胞死亡模式
Chin Med J (Engl). 2008 Oct 5;121(19):1920-4.
5
Exploring the full spectrum of macrophage activation.探索巨噬细胞激活的全谱。
Nat Rev Immunol. 2008 Dec;8(12):958-69. doi: 10.1038/nri2448.
6
Pancreatitis-associated protein 2 modulates inflammatory responses in macrophages.胰腺炎相关蛋白2调节巨噬细胞中的炎症反应。
J Immunol. 2008 Aug 1;181(3):1948-58. doi: 10.4049/jimmunol.181.3.1948.
7
Substance P enhances NF-kappaB transactivation and chemokine response in murine macrophages via ERK1/2 and p38 MAPK signaling pathways.P物质通过ERK1/2和p38丝裂原活化蛋白激酶信号通路增强小鼠巨噬细胞中的核因子κB反式激活及趋化因子反应。
Am J Physiol Cell Physiol. 2008 Jun;294(6):C1586-96. doi: 10.1152/ajpcell.00129.2008. Epub 2008 Apr 23.
8
Sphingosine-1-phosphate and its analogue FTY720 diminish acute pulmonary injury in rats with acute necrotizing pancreatitis.鞘氨醇-1-磷酸及其类似物FTY720可减轻急性坏死性胰腺炎大鼠的急性肺损伤。
Pancreas. 2008 Apr;36(3):e10-5. doi: 10.1097/MPA.0b013e31815f3905.
9
Sodium arsenite induces heat shock protein 70 expression and protects against secretagogue-induced trypsinogen and NF-kappaB activation.亚砷酸钠诱导热休克蛋白70表达并防止促分泌素诱导的胰蛋白酶原和核因子κB激活。
J Cell Physiol. 2008 Apr;215(1):37-46. doi: 10.1002/jcp.21286.
10
The role of NF-kappaB activation in the pathogenesis of acute pancreatitis.核因子-κB激活在急性胰腺炎发病机制中的作用。
Gut. 2008 Feb;57(2):259-67. doi: 10.1136/gut.2007.124115. Epub 2007 Aug 3.

单核细胞和巨噬细胞在急性胰腺炎进展中的重要作用。

Essential role of monocytes and macrophages in the progression of acute pancreatitis.

出版信息

World J Gastroenterol. 2010 Aug 28;16(32):3995-4002. doi: 10.3748/wjg.v16.i32.3995.

DOI:10.3748/wjg.v16.i32.3995
PMID:20731012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2928452/
Abstract

Acute pancreatitis (AP) is an inflammatory condition of the pancreas caused by an imbalance in factors involved in maintaining cellular homeostasis. Earliest events in AP occur within acinar cells accompanied by other principal contributors to the inflammatory response i.e. the endothelial cells, immunocytes (granulocytes, monocytes/macrophages, lymphocytes) and neutrophils. Monocytes/macrophages are important inflammatory mediators, involved in the pathophysiology of AP, known to reside in the peritoneal cavity (in the vicinity of the pancreas) and in peripancreatic tissue. Recent studies suggested that impaired clearance of injured acini by macrophages is associated with an altered cytokine reaction which may constitute a basis for progression of AP. This review focuses on the role of monocytes/macrophages in progression of AP and discusses findings on the inflammatory process involved.

摘要

急性胰腺炎(AP)是一种胰腺炎症性疾病,由维持细胞内稳态的因素失衡引起。AP 的最早事件发生在胰腺泡细胞内,同时伴有其他主要炎症反应的贡献者,即内皮细胞、免疫细胞(粒细胞、单核细胞/巨噬细胞、淋巴细胞)和中性粒细胞。单核细胞/巨噬细胞是重要的炎症介质,参与 AP 的病理生理学,已知存在于腹腔(胰腺附近)和胰周组织中。最近的研究表明,巨噬细胞清除受损胰腺泡的能力受损与细胞因子反应的改变有关,这可能是 AP 进展的基础。这篇综述重点讨论了单核细胞/巨噬细胞在 AP 进展中的作用,并讨论了涉及的炎症过程的发现。