Development for Anti-Cytokine Therapy on Hepatic Graft Reperfusion Injury.
肝移植物再灌注损伤的抗细胞因子疗法的发展。
基本信息
- 批准号:07407034
- 负责人:
- 金额:$ 9.22万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (A)
- 财政年份:1995
- 资助国家:日本
- 起止时间:1995 至 1996
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Inflammatory cytokines, interleukin (IL)-l and tumor necrosis factor (TNF), may play an important role in hepatic ischemia-reperfusion (I/R) injury. To study the role of IL-l in hepatic I/R injury, we investigated the effect of pretreatment with IL-l receptor antagonist (IL-1ra) on the production of IL-l and TNF,histological findings in the liver, and the survival rate for 7 days. The animals were subjected to 90 min of warm liver ischemia by clamping the portal vein and hepatic artery of the left and middle lobes. In the IL-lra-treated group, IL-lra was given 5 min before inducing liver ischemia. IL-la (ELISA) and TNF (L929) were determined in blood and liver at 0,30,90, and 180 min post-reperfusion. In addition, at 180 min post-reperfusion the damaged (left lateral and median lobes) and non-damaged (right lateral and caudate lobes) livers were removed respectively for IL-la and TNF determination. In another experiment to determine the effect of IL-lra pretreatment on survival rate fo … More r 7 days, after 90 min of liver ischemia, the vessels were released and the right lateral and caudate lobes were excised, leaving only the ischemic left lateral and median lobes. In both groups, IL-la was undetectable in blood, but was increased in liver tissue. TNF increased in both blood and liver tissue as reperfusion time increased. The histological findings were minimal in the IL-lra-treated group even at 180 min post-reperfusion. Furthermore, in the IL-lra-treated group, the production of TNF was decreased in both blood and liver tissue as compared with that in the non-treated group. At 180 min post-reperfusion, damaged liver produced significantly more IL-la and TNF than the non-damaged liver. Survival rates in the IL-lra-treated group and in the non-treated group were 80% (8/10) and 30% (6/20), respectively. The data demonstrated that the production of IL-l and TNF increases in hepatic I/R injury and that pretreatment with IL-lra protects the liver from ischemic insult, indicating the important role of IL-l in I/R injury. Less
炎性细胞因子白细胞介素(IL)-1和肿瘤坏死因子(TNF)在肝脏缺血再灌注损伤中起重要作用。为研究IL-1在肝I/R损伤中的作用,我们观察了IL-1受体拮抗剂(IL-1 ra)预处理对IL-1和TNF产生、肝脏组织学改变和7天存活率的影响。夹闭肝左、中叶门静脉和肝动脉,造成90 min的热肝缺血。IL-1 ra治疗组在诱导肝缺血前5 min给予IL-1 ra。分别于再灌注后0、30、90、180 min取血及肝组织,用ELISA法测定IL-1 α和TNF(L929)。此外,在再灌注后180分钟,分别取出受损(左外侧叶和中叶)和未受损(右外侧叶和尾状叶)的肝脏用于IL-1 α和TNF测定。在另一个实验中,为了确定IL-1 ra预处理对小鼠存活率的影响, ...更多信息 第7天,肝脏缺血90分钟后,释放血管,切除右侧叶和尾状叶,仅保留缺血的左侧叶和中间叶。在两组中,IL-1a在血液中检测不到,但在肝组织中增加。随着再灌注时间的延长,血和肝组织中TNF均升高。即使在再灌注后180分钟,IL-1 ra治疗组的组织学发现也是最小的。此外,在IL-1 ra治疗组中,与未治疗组相比,血液和肝组织中TNF的产生均减少。在再灌注后180分钟,受损肝脏产生比未受损肝脏显著更多的IL-1 α和TNF。IL-1 ra治疗组和未治疗组的存活率分别为80%(8/10)和30%(6/20)。数据表明,IL-1和TNF的产生在肝I/R损伤中增加,并且用IL-1 ra预处理保护肝脏免受缺血性损伤,表明IL-1在I/R损伤中的重要作用。少
项目成果
期刊论文数量(27)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
CARVALHO L.G.: "anti-IL-8 monoclonal antibody reduces free redical production and improves hemody namics and survival rate in rabbits" Surgery. (in press). (1997)
CARVALHO L.G.:“抗 IL-8 单克隆抗体减少了游离红的产生,改善了兔子的血流动力学和存活率”手术。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
島津元英: "生体部分肝移植と全身管理" Ope Nursing. 11. 26-32 (1996)
Motohide Shimazu:“活体部分肝移植和系统管理”OPE 护理。 11. 26-32 (1996)
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
若林 剛: "臓器微小循環障害の成因と意義" 日本外科学会雑誌. 97・9. 759-764 (1996)
若林刚:“器官微循环障碍的原因和意义”日本外科学会杂志97・9(1996)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
白杉 望: "生体部分肝移植後の血中サイトカイン変動とその意義" 消化器と免疫. 32・2. 171-175 (1996)
白杉希:“活体部分肝移植后血液细胞因子的变化及其意义”胃肠病学和免疫学 171-175(1996)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
KARAHASHI T.: "Rabbit real-time observation model of live ischemia-reperfusion" Microcirc Ann. 12. 141-142 (1996)
KARAHASHI T.:“活体缺血再灌注兔实时观察模型”Microcirc Ann。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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KITAJIMA Masaki其他文献
KITAJIMA Masaki的其他文献
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{{ truncateString('KITAJIMA Masaki', 18)}}的其他基金
Development of the new strategy in ABO blood group incompatible transplantation
ABO血型不合移植新策略的制定
- 批准号:
17209044 - 财政年份:2005
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Approaches to the clinical application of donor-specific tolerance in living donor organ transplantation.
供者特异性耐受在活体器官移植中的临床应用方法。
- 批准号:
14207049 - 财政年份:2002
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Development of novel minimally invasive surgery for solid tumors using sentinel node navigation
使用前哨节点导航开发新型实体瘤微创手术
- 批准号:
13357012 - 财政年份:2001
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Novel approach to control ischemia-reperfusion injury in small intestinal transplantation
控制小肠移植缺血再灌注损伤的新方法
- 批准号:
12307025 - 财政年份:2000
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Development of robotics-aided surgery system and tele-mentoring system in surgery
机器人辅助手术系统和远程手术指导系统的开发
- 批准号:
11357011 - 财政年份:1999
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A).
Anti-inflammatory cytokine gene transfection into allo graft organ
抗炎细胞因子基因转染同种异体移植器官
- 批准号:
09470257 - 财政年份:1997
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Development of surgical robotic system for extending the indication of advanced laparoscopic surgery.
开发手术机器人系统以扩展高级腹腔镜手术的适应症。
- 批准号:
07557085 - 财政年份:1995
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for Scientific Research (A)
Reperfusion Injury of the Liver and Stomach in Liver Transplant
肝移植中肝胃再灌注损伤
- 批准号:
04404053 - 财政年份:1992
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (A)
A experimental study on elucidation of developmental mechanism and treatment of stress ulcer from the viewpoint of gastric mucosal barrier.
从胃粘膜屏障的角度阐明应激性溃疡发生机制和治疗的实验研究。
- 批准号:
01480332 - 财政年份:1989
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)
Pathophysiology in the development of stress ulcer with special reference to gastric mucosal defensive mechanism.
应激性溃疡发展的病理生理学特别涉及胃粘膜防御机制。
- 批准号:
61571129 - 财政年份:1986
- 资助金额:
$ 9.22万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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