The role of the transcelluIar route and paracelluIar route in bacterial translocation
The role of the transcelluIar route and paracelluIar route in bacterial translocation
批准号:
21791293
负责人:
YOSHIKAWA Kozo
金额:
$2.75万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2009
资助国家:
日本
项目状态:
已结题
起止时间:
2009 至 2010
中文摘要
【背景】:本研究旨在阐明细菌易位中跨细胞和细胞旁途径可能参与的功能。【方法与结果】:1)经细胞途径:将10只wister大鼠分为两组,5只给予伊立替康治疗,5只不给予伊立替康治疗为对照组。伊立替康处理大鼠于第0、1天腹腔注射伊立替康250 mg/kg,给药后48 h处死,收集组织分析。对照组用生理盐水处理。BT组细胞凋亡增加,炎症因子升高。降低了大鼠的大肠阻力。2)细胞旁通路:细胞旁通路研究采用相同模型。伊立替康组大鼠小肠和大肠Claudin-1蛋白表达降低(P<0.05),小肠occludin蛋白表达降低(P<0.05),大肠occludin蛋白表达有降低趋势(P=0.07)。伊立替康组大鼠小肠claudin-1 mRNA表达降低(P<0.05),大肠claudin-1 mRNA表达有降低趋势(P=0.05),小肠和大肠occludin mRNA表达均降低(P<0.05)。3)自噬:我们使用Atg敲除小鼠(缺乏自噬功能)。小鼠给予伊立替康治疗。现在我们研究自噬功能与细菌易位之间的关系。【结论】:这些结果提示细菌易位与胞外途径和胞外途径有一定的关系。可能是这些机制阻止了细菌的易位。
英文摘要
【Background】 : This aim of this study was conducted to clarify the possible functional involvement of transcellular and paracellular route in bacterial translocation.【Methods and Results】 : 1) Transcellular route : Ten wister rats were divided into two groups : Five were treated with irinotecan and five were not treated with irinotecan, the control group. Irinotecan treated rats were administrated irinotecan 250 mg/kg intraperitoneally on days designated 0 and 1, were then killed at 48 h after treatment, and tissues were collected for analysis. Controls were treated with a saline solution. Apoptosis in the BT group was increased and inflammatory cytokine was also increased. Large intestinal resistance of the rats was decreased. 2) Paracellular route : Same model was adopted in paracellular route study. Claudin-1 protein expression of both the small and large intestine decreased (P<0.05), occludin protein expression of the small intestine decreased (P<0.05), and occludin protein expression of the large intestine had decreasing tendency (P=0.07) in irinotecan treated rats. In irinotecan treated rats, claudin-1 mRNA of the small intestine decreased (P<0.05), claudin-1 mRNA of large intestine had a tendency to decrease (P=0.05), occludin mRNA of both small and large intestine decreased (P<0.05). 3) Autophagy : We use the Atg knock out mouse (lacked the autophagy function). Mouse was treated with irinotecan. Now we investigate the relationship between the autophagy function and bacterial translocation.【Conclusions】 : Those findings indicated some relationship between the transcellular and paracellular route and bacterial translocation. It is possible that these mechanism prevent the bacterial translocation.
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Sonic hedgehog pathway in adenoma-carcinoma sequence.
腺瘤-癌序列中的声波刺猬通路。
DOI:
--
发表时间:
2009
期刊:
Journal of Gastroenterolgy 44
影响因子:
--
作者:
[Yoshikawa K, et al, Kozo Yoshikawa]
通讯作者:
Kozo Yoshikawa
Increased risk of lymph node metastasis in mucosal gastric cancer with extra indication for endoscopic mucosal resection
粘膜胃癌淋巴结转移的风险增加,有额外的内镜粘膜切除指征
DOI:
--
发表时间:
2009
期刊:
Journal of the American College of Surgeons 208
影响因子:
--
作者:
[Yoshikawa K, et al, Kozo Yoshikawa, Kozo Yoshikawa]
通讯作者:
Kozo Yoshikawa
CPT-11による腸管粘膜傷害と大建中湯の予防効果に関する研究
CPT-11引起的肠粘膜损伤及大健中汤的预防作用研究
DOI:
--
发表时间:
2009
期刊:
影响因子:
--
作者:
[Yoshikawa K, et al, Kozo Yoshikawa, Kozo Yoshikawa, Kozo Yoshikawa, 吉川幸造, 中尾寿宏, 中尾寿宏, 吉川幸造, 森本慎也]
通讯作者:
森本慎也
Increased risk of lymph node metastasis in mucosal gastric cancer with extra indication for endoscopic mucosal resection.
粘膜胃癌淋巴结转移的风险增加,有额外的内镜粘膜切除指征。
DOI:
--
发表时间:
2009
期刊:
J Am Coll Surg 208
影响因子:
--
作者:
[Yoshikawa K, et al]
通讯作者:
et al
Idiopathic phlebosclerosis : an atypical presentation of ischemic colitis treated by laparoscopic colectomy.
特发性静脉硬化症:通过腹腔镜结肠切除术治疗的缺血性结肠炎的非典型表现。
DOI:
--
发表时间:
2009
期刊:
Surgery 145
影响因子:
--
作者:
[Yoshikawa K, et al, Kozo Yoshikawa, Kozo Yoshikawa, Kozo Yoshikawa]
通讯作者:
Kozo Yoshikawa
共 11 条
The role of Sonic hedgehog in intestinal injury via stem cell
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批准号:25461951
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项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.24万
-
财政年份:2013
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负责人:YOSHIKAWA Kozo
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依托单位:
The role of sonic hedgehog signaling in intestinal injury
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批准号:23791536
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项目类别:Grant-in-Aid for Young Scientists (B)
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资助金额:$2.75万
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财政年份:2011
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负责人:YOSHIKAWA Kozo
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依托单位: