Sucralfate prevents the delay of wound repair in intestinal epithelial cells by hydrogen peroxide through NF-κB pathway
Sucralfate prevents the delay of wound repair in intestinal epithelial cells by hydrogen peroxide through NF-κB pathway
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硫糖铝通过 NF-κB 通路阻止过氧化氢延迟肠上皮细胞伤口修复
DOI：
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发表时间：
2006
影响因子：
6.3
通讯作者：
Sumio Watanabe
中科院分区：
文献类型：
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作者：
K. Shindo;M. Iizuka;K. Sasaki;S. Konno;H. Itou;Y. Horie;Sumio Watanabe
研究背景近年来研究表明硫糖铝（SF）对溃疡性结肠炎的结肠炎症有治疗作用。方法（1）用10−4 M蔗糖八硫酸钾（potassium sucrose octasulfate，SOS）刺激IEC-6细胞后，Western blot检测SF对IEC-6细胞信号蛋白[ERK 1/2 mitogen-activated protein kinase，MAPK，IκB-α]的激活。(2)采用逆转录聚合酶链反应（RT-PCR）检测SOS对IEC-6细胞转化生长因子（TGF）-β1、TGF-α、EGF和环氧合酶（考克斯-2）mRNA表达的影响。(3)将IEC-6细胞损伤并在不存在或存在20 μM H2 O2的情况下用不同浓度的SOS培养24 h。结果（1）SOS激活IκB-α，但不激活ERK 1/2 MAPK; (2)SOS可促进考克斯-2 mRNA的表达，但不影响其他生长因子mRNA的表达。(3)SOS并不增强IEC-6细胞的伤口修复，但它以剂量依赖性方式减少死亡细胞数量（最大，74%）（P < 0.01），并阻止H2 O2诱导的上皮迁移（最大，61%）（P < 0.01）和增殖（最大，37%）（P < 0.05）的减弱。结论SOS可能通过诱导考克斯-B和抗凋亡机制，阻止H2 O2诱导的IEC-6细胞创伤修复延迟。SOS的这些作用可能是通过激活NF-κB通路实现的。
BackgroundRecent studies have shown that sucralfate (SF) has therapeutic effects on colonic inflammation in ulcerative colitis. The aim of this study was to clarify the function of SF for wound repair in intestinal epithelial cells (IEC).Methods(1) Activation of signal proteins [ERK1/2 mitogen-activated protein kinase (MAPK), IκB-α] in IEC-6 cells after stimulation with 10−4 M potassium sucrose octasulfate (SOS), which is the functional element of SF, was assessed by Western blot. (2) Induction of transforming growth factor (TGF)-β1, TGF-α, EGF, and cyclooxygenase-2 (COX-2) mRNA after stimulation of IEC-6 cells with SOS was assessed by reverse transcriptase-polymerase chain reaction. (3) IEC-6 cells were wounded and cultured for 24 h with various concentrations of SOS in the absence or presence of 20 μM H2O2. Epithelial migration or proliferation was assessed by counting migrating cells or bromodeoxyuridine (BrdU)-positive cells across the wound border.Results(1) SOS activated IκB-α, but it did not activate ERK1/2 MAPK. (2) SOS enhanced the expression of COX-2 mRNA, but it did not change the mRNA expression of other growth factors. (3) SOS did not enhance wound repair in IEC-6 cells, but it decreased the number of dead cells (maximum, 74%) (P < 0.01) in a dose-dependent manner and prevented the diminishment of epithelial migration (maximum, 61%) (P < 0.01) and proliferation (maximum, 37%) (P < 0.05) induced by H2O2. These functions of SOS were suppressed by the NF-κB and COX-2 inhibitors.ConclusionsSOS prevented the delay of wound repair in IEC-6 cells induced by H2O2, probably through induction of COX-2 and an anti-apoptotic mechanism. These effects of SOS might be given through the activation of the NF-κB pathway.
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影响因子：
29.4
作者：
Göke, M;Kanai, M;Podolsky, DK
通讯作者：
Podolsky, DK
影响因子：
11.2
作者：
H. Sheng;J. Shao;J. Morrow;R. Beauchamp;R. Dubois
通讯作者：
H. Sheng;J. Shao;J. Morrow;R. Beauchamp;R. Dubois
影响因子：
7.4
作者：
Denning, TL;Takaishi, H;Ernst, PB
通讯作者：
Ernst, PB
影响因子：
--
作者：
MCCORMACK, SA;VIAR, MJ;JOHNSON, LR
通讯作者：
JOHNSON, LR