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1
Glycogen synthase kinase-3beta inhibition attenuates the degree of arthritis caused by type II collagen in the mouse.糖原合酶激酶-3β抑制可减轻小鼠中由II型胶原引起的关节炎程度。
Clin Immunol. 2006 Jul;120(1):57-67. doi: 10.1016/j.clim.2006.03.005. Epub 2006 May 2.
2
Glycogen synthase kinase-3 beta inhibition reduces secondary damage in experimental spinal cord trauma.糖原合酶激酶-3β抑制可减轻实验性脊髓损伤中的继发性损伤。
J Pharmacol Exp Ther. 2006 Jul;318(1):79-89. doi: 10.1124/jpet.106.102863. Epub 2006 Apr 6.
3
Reduction of experimental colitis in the rat by inhibitors of glycogen synthase kinase-3beta.糖原合成酶激酶-3β抑制剂减轻大鼠实验性结肠炎
Br J Pharmacol. 2006 Mar;147(5):575-82. doi: 10.1038/sj.bjp.0706509.
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Glycogen synthase kinase 3beta functions to specify gene-specific, NF-kappaB-dependent transcription.糖原合酶激酶3β负责特定基因的、依赖核因子-κB的转录过程。
Mol Cell Biol. 2005 Oct;25(19):8444-55. doi: 10.1128/MCB.25.19.8444-8455.2005.
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GSK-3beta inhibitors attenuate the organ injury/dysfunction caused by endotoxemia in the rat.糖原合成酶激酶-3β抑制剂可减轻大鼠内毒素血症所致的器官损伤/功能障碍。
Crit Care Med. 2005 Sep;33(9):1903-12. doi: 10.1097/01.ccm.0000178350.21839.44.
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Toll-like receptor-mediated cytokine production is differentially regulated by glycogen synthase kinase 3.Toll样受体介导的细胞因子产生受糖原合酶激酶3的差异调节。
Nat Immunol. 2005 Aug;6(8):777-84. doi: 10.1038/ni1221. Epub 2005 Jul 10.
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Tumour necrosis factor receptor gene therapy affects cellular immune responses in collagen induced arthritis in mice.肿瘤坏死因子受体基因疗法影响小鼠胶原诱导性关节炎中的细胞免疫反应。
Ann Rheum Dis. 2005 Nov;64(11):1550-6. doi: 10.1136/ard.2004.025619. Epub 2005 Apr 28.
8
Nuclear factor (NF)-kappaB proteins: therapeutic targets.核因子（NF）-κB蛋白：治疗靶点。
Ann Rheum Dis. 2004 Nov;63 Suppl 2(Suppl 2):ii57-ii61. doi: 10.1136/ard.2004.028266.
9
Phosphorylation of serine 468 by GSK-3beta negatively regulates basal p65 NF-kappaB activity.GSK-3β对丝氨酸468的磷酸化负向调节基础p65核因子κB活性。
J Biol Chem. 2004 Nov 26;279(48):49571-4. doi: 10.1074/jbc.C400442200. Epub 2004 Oct 1.
10
Genetic deletion of glycogen synthase kinase-3beta abrogates activation of IkappaBalpha kinase, JNK, Akt, and p44/p42 MAPK but potentiates apoptosis induced by tumor necrosis factor.糖原合酶激酶-3β的基因缺失可消除IκBα激酶、JNK、Akt和p44/p42丝裂原活化蛋白激酶的激活，但增强肿瘤坏死因子诱导的细胞凋亡。
J Biol Chem. 2004 Sep 17;279(38):39541-54. doi: 10.1074/jbc.M403449200. Epub 2004 Jul 13.

糖原合酶激酶-3β的抑制作用可减轻角叉菜胶诱导的小鼠肺损伤的发展。

Inhibition of glycogen synthase kinase-3beta attenuates the development of carrageenan-induced lung injury in mice.

作者信息

Cuzzocrea S, Crisafulli C, Mazzon E, Esposito E, Muià C, Abdelrahman M, Di Paola R, Thiemermann C

机构信息

Department of Clinical and Experimental Medicine and Pharmacology, School of Medicine, University of Messina, Messina, Italy.

出版信息

Br J Pharmacol. 2006 Nov;149(6):687-702. doi: 10.1038/sj.bjp.0706902. Epub 2006 Oct 3.

DOI:10.1038/sj.bjp.0706902
PMID:17016509
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2014652/
Abstract

BACKGROUND AND PURPOSE

Glycogen synthase kinase-3 (GSK-3) is a ubiquitous serine-threonine protein kinase that participates in a multitude of cellular processes and has recently been implicated in the pathophysiology of a number of diseases. The aim of this study was to investigate the effects of GSK-3beta inhibition in a model of acute inflammation. Here, we have investigated the effects of TDZD-8, a potent and selective GSK-3beta inhibitor, in a mouse model of carrageenan-induced pleurisy.

EXPERIMENTAL APPROACH

Injection of carrageenan into the pleural cavity of mice elicited an acute inflammatory response characterized by: accumulation of fluid containing a large number of neutrophils (PMNs) in the pleural cavity, infiltration of PMNs in lung tissues and subsequent lipid peroxidation, and increased production of nitrite/nitrate (NOx), prostaglandin E2 (PGE2), tumour necrosis factor-alpha, (TNF-alpha) and interleukin-1beta (IL-1beta). Furthermore, carrageenan induced an upregulation of the adhesion molecules ICAM-1 and P-selectin, iNOS, COX-2 as well as nitrotyrosine as determined by immunohistochemical analysis of lung tissues.

KEY RESULTS

Administration of TDZD-8 (1, 3 or 10 mg kg(-1), i.p.), 30 min prior to injection of carrageenan, caused a dose-dependent reduction in all the parameters of inflammation measured.

CONCLUSIONS AND IMPLICATIONS

Thus, based on these findings we propose that inhibitors of the activity of GSK-3beta, such as TDZD-8, may be useful in the treatment of various inflammatory diseases.

摘要

背景与目的

糖原合酶激酶-3（GSK-3）是一种普遍存在的丝氨酸-苏氨酸蛋白激酶，参与多种细胞过程，最近被认为与多种疾病的病理生理学有关。本研究的目的是在急性炎症模型中研究GSK-3β抑制的作用。在此，我们研究了强效选择性GSK-3β抑制剂TDZD-8在角叉菜胶诱导的小鼠胸膜炎模型中的作用。

实验方法

向小鼠胸腔内注射角叉菜胶引发急性炎症反应，其特征为：胸腔内积聚含有大量中性粒细胞（PMN）的液体，PMN浸润肺组织并随后发生脂质过氧化，以及亚硝酸盐/硝酸盐（NOx）、前列腺素E2（PGE2）、肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的产生增加。此外，通过对肺组织进行免疫组织化学分析确定，角叉菜胶诱导了黏附分子ICAM-1和P-选择素、诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）以及硝基酪氨酸的上调。

关键结果

在注射角叉菜胶前30分钟腹腔注射TDZD-8（1、3或10 mg kg⁻¹），导致所测所有炎症参数呈剂量依赖性降低。

结论与意义

因此，基于这些发现我们提出，GSK-3β活性抑制剂，如TDZD-8，可能对治疗各种炎症性疾病有用。