Effect of food-derived intestinal content such as fatty acids on intestinal mucosal barrier
脂肪酸等食物来源的肠道内容物对肠粘膜屏障的影响
基本信息
- 批准号:10670518
- 负责人:
- 金额:$ 0.32万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1998
- 资助国家:日本
- 起止时间:1998 至 1999
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
1. Effect of nitric oxide (NO) on intestinal epithelial permeability and tight junction protein (occludin)NO donors increased the permeability of the Caco-2 cell monolayer. NOS inhibitors suppressed taurocholate-induced hyperpermeability. In the presence of NO donor, fluorescence was observed at the paracellular space one hour after the addition of FITC-dextran to the apical compartment. In the presence of NO donor, the higher molecular-weight band of occludin became faint. In the presence of NO donor, bands obtained using anti-phophoserine antibody corresponding with the higher molecular-weight band of occuludin became faint. In the presence of NO donor, occludin was stained at the tight junction but the stain was a little broader than that in the control. These findings suggested that intestinal epithelial permeability is increased not only by exogenously administered NO but also by NO produced by intestinal epithelial cells. The increased permeability appears to be due to the dilati … More on of the tight junction, which is associated with the dephosphorylation of occuludin.2. Effect of fatty acids on chemokine production in intestinal epithelial cells, Caco-2 cellsButyate, short-chain fatty acid, decreased interleukin(IL)-8 production in intestinal epithelial cells.ω-3 fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) showed no effect on IL-8 production. Oleic acid (OA) and capric acid (CA) increased IL-8 production. Proteainkinase C and phospholipase A2 were involved in signal transduction pathways for OA-induced IL-8 production but not for CA-induced IL-8 production.3. Measurement of proteins in whole gut lavage fluid (WGLF) and fecesEither WGLF or feces can be used as a sample to investigate pathophysiology and disease activity in patients with inflammatory bowel disease (IBD). In active IBD, the concentrations of granular proteins were increased both in the supernatant and pellet, and the supernatant/pellet ratios of granular proteins were decreased. These findings suggested that although the migration of neutrophils into the lumen is extremely increased in active IBD, a number of neutrophils that migrated into the lumen did not release granular proteins. Less
1. 一氧化氮(NO)对肠上皮通透性的影响和紧密连接蛋白(occludin)NO供体增加Caco-2细胞单层通透性。NOS抑制剂抑制牛磺胆酸诱导的高通透性。在NO供体存在的情况下,将fitc -葡聚糖加入根尖室1小时后,在细胞旁间隙观察荧光。在NO供体存在时,occludin的高分子量带变得微弱。在NO供体存在的情况下,与暗蛋白高分子量条带对应的抗磷酸丝氨酸抗体获得的条带变暗。在NO供体存在的情况下,occludin在紧密连接处染色,但染色比对照组稍宽。这些结果表明,肠道上皮细胞的通透性不仅可以通过外源性NO增加,还可以通过肠道上皮细胞产生的NO增加。通透性的增加似乎是由于紧密连接的扩张,这与隐性蛋白的去磷酸化有关。脂肪酸对肠上皮细胞趋化因子生成的影响,Caco-2细胞丁酸,短链脂肪酸,降低肠上皮细胞白细胞介素(IL)-8的生成。ω-3脂肪酸如二十二碳六烯酸(DHA)和二十碳五烯酸(EPA)对IL-8的产生没有影响。油酸(OA)和癸酸(CA)增加了IL-8的产量。蛋白激酶C和磷脂酶A2参与了oa诱导的IL-8产生的信号转导途径,但不参与ca诱导的IL-8产生的信号转导途径。全肠灌洗液(WGLF)和粪便中蛋白质的测定WGLF或粪便均可作为研究炎症性肠病(IBD)患者病理生理和疾病活动性的样本。在活动性IBD中,颗粒蛋白在上清液和球团中的浓度均增加,颗粒蛋白的上清/球团比降低。这些发现表明,尽管中性粒细胞在活动性IBD中迁移到管腔的数量急剧增加,但许多迁移到管腔的中性粒细胞并没有释放颗粒蛋白。少
项目成果
期刊论文数量(36)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Saitoh O, Sugi K, Kojima K, et al.: "Increased prevalence of intestinal inflammation in patients with liver cirrhosis"World J Gastroenterology. 5(5). 391-396 (1999)
Saitoh O、Sugi K、Kojima K 等人:“肝硬化患者肠道炎症患病率增加”《世界胃肠病学杂志》。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Osamu Saitoh: "Bile acids inhibit tumor necroscs factor-α-induced interleukin-8 production in human colon epithelial cells." J Gastroenterol Hepatol. 13. 1212-1217 (1998)
Osamu Saitoh:“胆汁酸抑制人结肠上皮细胞中肿瘤坏死因子-α 诱导的白细胞介素 8 的产生。”J Gastroenterol Hepatol。13. 1212-1217 (1998)
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
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- 通讯作者:
Matsumoto A, Saitoh O., Matsumoto H, et al.: "Acquired ileal diverticulum: an unusual bleeding source"J. Gastroenterol.. 35. 163-167 (2000)
Matsumoto A、Saitoh O.、Matsumoto H 等人:“获得性回肠憩室:一种不寻常的出血源”J.
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Sugi K, et al.: "Antineutrophil cytoplasmic antibodies in Japanese patients with inflammatory bowel disease"Am J Gastroenterol. 94. 1304-1312 (1999)
Sugi K 等人:“日本炎症性肠病患者的抗中性粒细胞胞浆抗体”Am J Gastroenterol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
井尻 好雄 他: "過敏性腸症候群の治療.消化器疾患の薬物療法-処方解説"日本薬剤師研修センター. 63-87 (1999)
Yoshio Ijiri 等:“肠易激综合症的治疗。胃肠道疾病的药物治疗 - 处方说明”日本药剂师培训中心 63-87 (1999)。
- DOI:
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- 影响因子:0
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SAITOH Osamu其他文献
SAITOH Osamu的其他文献
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{{ truncateString('SAITOH Osamu', 18)}}的其他基金
Auto-oxidation products of epigallocatechin gallate activate TRPA1 and TRPV1 in sensory neurons.
表没食子儿茶素没食子酸酯的自动氧化产物激活感觉神经元中的 TRPA1 和 TRPV1。
- 批准号:
24570170 - 财政年份:2012
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The membrane-target mechanism of taste receptors
味觉受体的膜靶机制
- 批准号:
18570138 - 财政年份:2006
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The molecular mechanism for receptor specific suppression of Gq system by RGS8
RGS8受体特异性抑制Gq系统的分子机制
- 批准号:
15570132 - 财政年份:2003
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular Mechanism of activity dependent translocation of RGS8
RGS8活性依赖性易位的分子机制
- 批准号:
13680730 - 财政年份:2001
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Effect of fatty acids on injury and repair of intestinal mucosal barrier
脂肪酸对肠粘膜屏障损伤与修复的影响
- 批准号:
12670531 - 财政年份:2000
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular Mechanism Controlling Acceleration Patterns of G-protein Signaling Induced by RGS Proteins.
控制 RGS 蛋白诱导的 G 蛋白信号传导加速模式的分子机制。
- 批准号:
11680647 - 财政年份:1999
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Pathophysiology of disrupted intestinal mucosal barrier (increased permeability and protein loss)
肠粘膜屏障破坏的病理生理学(渗透性增加和蛋白质损失)
- 批准号:
07670630 - 财政年份:1995
- 资助金额:
$ 0.32万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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