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Experimental Research for Regeneration of damaged Liver

受损肝脏再生的实验研究

基本信息

批准号：
06454366
负责人：
UEMOTO Shinji
金额：
$ 3.26万
依托单位：
KYOTO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

项目摘要

1.In the hepatectomized patients, binding capacity of lymphocyte beta2-adrenoreceptor was assayd in relation to changes in arterial blood ketone body ratio (AKBR) presenting mitochondrial redox potential. In the low post-operative AKBR group, postoperative maximum biding capacity of lymphocyte beta2-adrenoreceptor (Bmax) decreased more that in the high AKBR group. It was suggested that the surgical stress produced by hepatectomy may influence the ligand-receptor binding capacity, and that AKBR can indicate the magnitude of surgical stress.2.The effects of extracellular FK binding protein 12 (FKBP12) were studied in vitro and in patients received liver transplantation. FKBP12 inhibited the ability of FK506 (immuno-suppressive agent) to suppress phytohem-agglutinin-induced proliferative response of human peripheral blood mono-nuclear cells. Clinically, the rapid increase in plasma level of FKBP12 may contribute to the occurrence and progress of acute cellular rejection, probably due to inhibition of the immunosuppressive activity of FK506.3.The effects of transient non-lethal hypoxia on epidermal growth factor (EGF) -induced DNA synthesis of rat hepatocytes were investigated. Transient hypoxia decreased intracellular ATP content, but reoxygenation restored the decrease in ATP.Such a hypoxia decreased the number of available EGF receptors without affecting the receptor protein expression, and inhibited the EGF-induced DNA aynthesis of rat hepatocytes through reversible changes in the EGF receptor molecule.

1.在肝切除患者中，测定淋巴细胞β -肾上腺素受体的结合能力与呈现线粒体氧化还原电位的动脉血酮体比（AKBR）变化的关系。低AKBR组术后淋巴细胞β -肾上腺素受体（Bmax）最大抑制能力比高AKBR组下降更明显。提示肝切除术产生的手术应激可能影响配体-受体结合能力，AKBR可反映手术应激的大小。研究了细胞外FK结合蛋白12 （FKBP12）在体外和肝移植患者中的作用。FKBP12抑制FK506（免疫抑制剂）抑制植物凝血素诱导的人外周血单核细胞增殖反应的能力。临床上，血浆中FKBP12水平的快速升高可能与急性细胞排斥反应的发生和进展有关，这可能与FK506.3的免疫抑制活性受到抑制有关。研究了短暂非致死缺氧对表皮生长因子（EGF）诱导的大鼠肝细胞DNA合成的影响。短暂缺氧使细胞内ATP含量降低，但再氧化恢复了ATP的减少。这种缺氧在不影响受体蛋白表达的情况下减少了可用EGF受体的数量，并通过EGF受体分子的可逆变化抑制了EGF诱导的大鼠肝细胞DNA合成。