Kupffer cells modulate splenic, interleukin-10 production in endotoxin-induced liver injury after partial hepatectomy.

部分肝切除术后内毒素诱导的肝损伤中，库普弗细胞调节脾脏、白细胞介素 10 的产生。

基本信息

批准号：
12671218
负责人：
NAKAMURA Toshio
金额：
$ 1.73万
依托单位：
Hamamatsu University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

Background : This study was conducted to investigate the implication of Kupffer cells and the spleen in interleukin (IL)-10 production in endotoxin-induced liver injury after hepatectomy.Materials and Methods : Rats were divided into five groups : the S group, sham-operation ; the SG group, sham-operation followed by intravenous gadolinium chloride (GdCl3 : 7mg/kg) administration to inhibit Kupffer cell function ; the H group, two-thirds hepatectomy ; the HG group, hepatectomy and subsequent GdCl3 administration ; the HGS group, hepatectomy and splenectomy with GdCl3 administration.Lipopolysaccharide (1.5mg/kg) was intravenously administered for each group 48 hours after surgery. Results : GdCl3 treatment significantly suppressed the elevation of plasma alanine aminotransferase and tumor necrosis factor (TNF)-a by lipopolysaccharide administration, and completely inhibited the induction of hepatic tissue TNF-a and IL-10 mRNAs. In the HG group, plasma IL-10 levels were significantly higher than those in the H and HGS groups and splenic IL-10 mRNA was markedly enhanced 1 hour after lipopolysaccharide administration. Plasma TNF-a /IL-10 ratio was higher in the rank order H>HGS>HG. The 24-hour mortality (H group, 67% ; HGS group, 33% ; HG group, 20%) and hepatic parenchymal damage was in the same order. Conclusion : Kupffer cells after hepatectomy may aggravate endotoxin-induced liver injury via down-regulation of IL-10 production in the spleen.

背景：进行了这项研究以研究kupffer细胞和脾脏在白介素（IL）-10产生肝切除术后内毒素诱导的肝损伤中的含义。材料和方法：将大鼠分为五组：S组，假手术； SG组，假手术，然后是静脉注射氯化静脉内（GDCL3：7mg/kg），以抑制kupffer细胞功能； H组，三分之二的肝切除术； HG组，肝切除术和随后的GDCL3给药； HGS组，肝切除术和脾切除术对GDCL3给药。脂肪糖（1.5mg/kg）在手术后48小时静脉内给予每组静脉内给药。结果：GDCL3治疗可显着抑制血浆氨基转移酶和肿瘤坏死因子（TNF）-A的升高，通过脂多糖给药，并完全抑制肝组织TNF-A和IL-10 mRNA的诱导。在HG组中，血浆IL-10水平明显高于H和HGS组中的血浆IL-10水平，并且在脂多糖给药后1小时显着增强了脾脏IL-10 mRNA。等离子TNF-A /IL-10比率较高，在等级顺序H> Hgs> Hg。 24小时的死亡率（H组为67％； HGS组，33％； HG组，20％）和肝实质损伤的顺序相同。结论：肝切除术后的库普弗细胞可能通过下调脾脏的IL-10产生而加剧内毒素诱导的肝损伤。