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本文引用的文献

1
Nitric oxide, cell signaling and cell death.一氧化氮、细胞信号传导与细胞死亡。
Toxicology. 2005 Mar 15;208(2):177-92. doi: 10.1016/j.tox.2004.11.032.
2
Highly selective inhibition of inducible nitric oxide synthase ameliorates experimental acute pancreatitis.诱导型一氧化氮合酶的高度选择性抑制可改善实验性急性胰腺炎。
Pancreas. 2005 Jan;30(1):e10-5.
3
Early events in acute pancreatitis.急性胰腺炎的早期事件
Gastroenterol Clin North Am. 2004 Dec;33(4):717-31. doi: 10.1016/j.gtc.2004.07.009.
4
Pancreatic two P domain K+ channels TALK-1 and TALK-2 are activated by nitric oxide and reactive oxygen species.胰腺双P结构域钾通道TALK-1和TALK-2可被一氧化氮和活性氧激活。
J Physiol. 2005 Jan 1;562(Pt 1):235-44. doi: 10.1113/jphysiol.2004.071266. Epub 2004 Oct 28.
5
Cholecystokinin-8-induced hypoplasia of the rat pancreas: influence of nitric oxide on cell proliferation and programmed cell death.胆囊收缩素-8诱导的大鼠胰腺发育不全:一氧化氮对细胞增殖和程序性细胞死亡的影响
Basic Clin Pharmacol Toxicol. 2004 Oct;95(4):183-90. doi: 10.1111/j.1742-7843.2004.pto_950406.x.
6
Protection against acute pancreatitis by activation of protease-activated receptor-2.通过激活蛋白酶激活受体-2预防急性胰腺炎
Am J Physiol Gastrointest Liver Physiol. 2005 Feb;288(2):G388-95. doi: 10.1152/ajpgi.00341.2004. Epub 2004 Sep 30.
7
Reduction in the development of cerulein-induced acute pancreatitis by treatment with M40401, a new selective superoxide dismutase mimetic.新型选择性超氧化物歧化酶模拟物M40401治疗可减少雨蛙肽诱导的急性胰腺炎的发生。
Shock. 2004 Sep;22(3):254-61. doi: 10.1097/01.shk.0000132490.79498.11.
8
Protective effects of L-arginine on reperfusion injury after pancreaticoduodenal transplantation in rats.L-精氨酸对大鼠胰十二指肠移植后再灌注损伤的保护作用。
Hepatobiliary Pancreat Dis Int. 2004 Aug;3(3):349-54.
9
Exogenous and endogenous nitric oxide donors improve post-ischemic tissue oxygenation in early pancreatic ischemia/reperfusion injury in the rat.外源性和内源性一氧化氮供体可改善大鼠早期胰腺缺血/再灌注损伤后缺血组织的氧合。
Eur Surg Res. 2004 Jul-Aug;36(4):219-25. doi: 10.1159/000078856.
10
L-arginine-induced experimental pancreatitis.L-精氨酸诱导的实验性胰腺炎。
World J Gastroenterol. 2004 Jul 15;10(14):2003-9. doi: 10.3748/wjg.v10.i14.2003.

自由基与胰腺腺泡细胞:在生理和病理中的作用

Free radicals and the pancreatic acinar cells: role in physiology and pathology.

作者信息

Chvanov M, Petersen O H, Tepikin A

机构信息

The University of Liverpool The Physiological Laboratory Crown Street, Liverpool L69 3BX, UK.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2005 Dec 29;360(1464):2273-84. doi: 10.1098/rstb.2005.1757.

DOI:10.1098/rstb.2005.1757
PMID:16321797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1569596/
Abstract

Reactive oxygen and nitrogen species (ROS and RNS) play an important role in signal transduction and cell injury processes. Nitric oxide synthase (NOS)-the key enzyme producing nitric oxide (NO)-is found in neuronal structures, vascular endothelium and, possibly, in acinar and ductal epithelial cells in the pancreas. NO is known to regulate cell homeostasis, and its effects on the acinar cells are reviewed here. ROS are implicated in the early events within the acinar cells, leading to the development of acute pancreatitis. The available data on ROS/RNS involvement in the apoptotic and necrotic death of pancreatic acinar cells will be discussed.

摘要

活性氧和氮物种(ROS和RNS)在信号转导和细胞损伤过程中起重要作用。一氧化氮合酶(NOS)——产生一氧化氮(NO)的关键酶——存在于神经元结构、血管内皮中,可能还存在于胰腺的腺泡和导管上皮细胞中。已知NO可调节细胞内稳态,本文将综述其对腺泡细胞的影响。ROS与腺泡细胞内的早期事件有关,可导致急性胰腺炎的发生。本文将讨论ROS/RNS参与胰腺腺泡细胞凋亡和坏死性死亡的现有数据。