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The modulation of transcription factor in liver regeneration after hepatic ischemia/reperfusion injury

The modulation of transcription factor in liver regeneration after hepatic ischemia/reperfusion injury
转录因子在肝缺血/再灌注损伤后肝再生中的调控
批准号:
15591381
负责人:
KATO Atsushi
金额:
$2.24万
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:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004

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1.Liver regeneration after hepatic ischemia/reperfusion injury.Although there is abundant evidence to support the mechanisms of hepatic ischemia/reperfusion, much less is known about the role of regeneration of the liver after ischemia/reperfusion. I used C57BL/6 mice to assess the function of activin-follistatin system in hepatic regeneration after ischemia and reperfusion injury. The expression of mRNA for activin during a time course of liver ischemia/reperfusion was determined by real time PCR methods. Activin expression was increased within 1 hour of reperfusion. Serum levels of activin were also increased after early time point of reperfusion. Follistatin protein levels in serum samples increased just after activin protein levels. These results indicate that activin inhibits initiation of regeneration in hepatocytes at early time point after hepatic ischemia/reperfusion. The activin-follistatin system is one of the important regulatory systems modulating regeneration processes of … More the liver. Endogenous interleukin-13 protects hepatocytes and vascular endothelial cells during ischemia/reperfusion injury. Thus, an alternative possibility is that IL-13 directly regulates regeneration of the liver through hepatocytes and endothelial cells function.2.Hepatic ischemia/reperfusion injury alterations in experimental cholestasis.Previous studies from our laboratory have established that obstructive jaundice can increase the neutrophil infiltrates into the liver and significantly elevate hepatoceLLular injury after hepatic ischemia/reperfusion. Male C57BL/6 mice underwent ligation and division of the common bile duct to make obstructive jaundice. Obstructive jaundice mice are far more susceptible to 90 minutes ischemia than 30 minutes ischemia 7 day after surgery. NFκB activation and subsequent production of proinflammatory cytokines such as TNF-α were dramatically increased in obstructive jaundice mice in early time point after hepatic ischemia/reperfusion compared to sham controls. These findings demonstrate that obstructive jaundice develops inflammatory cascade through NFκB activation and renders liver susceptible to hepatic ischemia/reperfusion.3.Clinical examination of hepatic ischemia/reperfusion injuryPostopertive levels of interleukin-6,interleukin-10,macrophage chemoattractant protein-1 and long hepatic ischemia were significantly correlated with postoperative surgical site infection and hepatocellular damage. Hepatic ischemia/reperfusion injury is potentially involved in the pathophysiology of postoperative infection and organ dysfunction. Less
期刊论文(22)
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Interleukin 18 causes hepatic ischemia/repefusion injury by suppressing anti-inflammatory cytokine expression in mice
白细胞介素18通过抑制小鼠抗炎细胞因子表达引起肝缺血/再灌注损伤
DOI: --
发表时间: 2004
期刊: Hepatology 39
影响因子: --
作者: [Takeuchi D, Kato A, et al.]
通讯作者: et al.
DOI: 10.1016/j.amjsurg.2003.08.029
发表时间: 2004-06-01
期刊: AMERICAN JOURNAL OF SURGERY
影响因子: 3
作者: [Kimura, F, Itoh, H, Miyazaki, M]
通讯作者: Miyazaki, M
Yoshidome H, Kato A, Miyazaki M.et al.: "Surgical treatment for extrahepatic recurrence after hepatectomy for colorectal metastases."Hepatogastroenterology. (in press).
Yoshidome H、Kato A、Miyazaki M.等:“结直肠转移肝切除术后肝外复发的手术治疗。”肝胃肠病学。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
Kato A, et al.: "Endogenous IL-13 protects hepatocytes and vascular endothelial cells during ischemia/reperfusion injury"Hepatology. .37. 304-312 (2003)
Kato A 等人:“内源性 IL-13 在缺血/再灌注损伤期间保护肝细胞和血管内皮细胞”肝病学。
DOI: --
发表时间:
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影响因子: --
作者: []
通讯作者:
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