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】:本研究的目的是阐明跨细胞和细胞旁途径在细菌移位中可能的功能参与。【方法与结果】:1)跨细胞途径:将10只wister大鼠分为两组:5只接受伊立替康治疗,5只未接受伊立替康治疗(对照组)。在指定的第0天和第1天,伊立替康给药大鼠腹腔内给予伊立替康250 mg/kg,然后在给药后48 h处死,采集组织进行分析。对照组用生理盐水处理。BT组细胞凋亡增加,炎性细胞因子也增加。大鼠大肠阻力降低。2)细胞旁途径:细胞旁途径研究采用相同模型。伊立替康组大鼠小肠和大肠Claudin-1蛋白表达均降低(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)。用伊立替康处理小鼠。现就自噬功能与细菌移位的关系进行研究。[结论]细菌的跨细胞和旁细胞途径与细菌移位有一定的关系。这些机制可能阻止细菌移位。
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)
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资助金额:$3.24万
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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: