• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

库普弗细胞在脓毒症期间肝功能障碍发展中的作用。

The role of Kupffer cells in the development of hepatic dysfunction during sepsis.

作者信息

Meng X J, Qiu B A, Li X J, Song X H

机构信息

Institute of Basic Medical Sciences, General Hospital of PLA, Beijing.

出版信息

Chin Med J (Engl). 1992 Jan;105(1):34-8.

PMID:1576868
Abstract

The effect of Kupffer cell blockade on hepatic function during sepsis was evaluated in this study. Methyl palmitate suspension 100 mg/100 g administered intravenously suppressed the phagocytic activity as the phagocytic index K decreased from 0.0493 +/- 0.0089 to 0.0150 +/- 0.0035 in rats. Sepsis was produced by the method of cecal ligation and needling perforation (CLP). At the end of 15 hours after CLP the hepatic adenosine triphosphate (ATP) level and ketone body ratio decreased significantly. But in rats pretreated with methyl palmitate 24 hours prior to CLP, the ATP level returned to the normal control level (1.6906 +/- 0.06-2.2323 +/- 0.13 mumol/g) and ketone body ratio remained at significantly higher values (0.26 to 0.68). After CLP, the liver lipoperoxide (LPO) concentration increased and glutathione (GSH) contents decreased significantly. When the septic rats were pretreated with methyl palmitate, both the LPO and GSH returned to the normal control level (62.69 +/- 1.7 to 44.62 +/- 2.12 and 159.85 +/- 9.7 to 222.27 +/- 11.34). It is concluded that the hepatic dysfunction is modulated at least to a greater extent by many of the toxic mediators released by the activated Kupffer cells during sepsis.

摘要

本研究评估了库普弗细胞阻断对脓毒症期间肝功能的影响。静脉注射100mg/100g的棕榈酸甲酯悬浮液可抑制吞噬活性,大鼠的吞噬指数K从0.0493±0.0089降至0.0150±0.0035。采用盲肠结扎穿刺(CLP)法制造脓毒症模型。CLP术后15小时末,肝脏三磷酸腺苷(ATP)水平和酮体比率显著降低。但在CLP前24小时用棕榈酸甲酯预处理的大鼠中,ATP水平恢复到正常对照水平(1.6906±0.06 - 2.2323±0.13μmol/g),酮体比率仍显著高于正常水平(0.26至0.68)。CLP后,肝脏脂质过氧化物(LPO)浓度升高,谷胱甘肽(GSH)含量显著降低。当脓毒症大鼠用棕榈酸甲酯预处理后,LPO和GSH均恢复到正常对照水平(62.69±1.7至44.62±2.12以及159.85±9.7至222.27±11.34)。得出的结论是,脓毒症期间活化的库普弗细胞释放的许多毒性介质至少在很大程度上调节了肝功能障碍。

相似文献

1
The role of Kupffer cells in the development of hepatic dysfunction during sepsis.库普弗细胞在脓毒症期间肝功能障碍发展中的作用。
Chin Med J (Engl). 1992 Jan;105(1):34-8.
2
Hepatic neutrophil sequestration in early sepsis: enhanced expression of adhesion molecules and phagocytic activity.早期脓毒症时肝脏中性粒细胞隔离:黏附分子表达增强及吞噬活性增强。
Shock. 1994 Aug;2(2):133-40.
3
Methyl palmitate: inhibitor of phagocytosis in primary rat Kupffer cells.棕榈酸甲酯:原代大鼠库普弗细胞吞噬作用的抑制剂。
Toxicology. 2005 Jun 1;210(2-3):197-204. doi: 10.1016/j.tox.2005.02.001.
4
Kupffer cell ablation attenuates cyclooxygenase-2 expression after trauma and sepsis.库普弗细胞消融可减轻创伤和脓毒症后环氧合酶-2的表达。
J Surg Res. 2005 Mar;124(1):126-33. doi: 10.1016/j.jss.2004.09.011.
5
Effects of methyl palmitate on cytokine release, liver injury and survival in mice with sepsis.棕榈酸甲酯对脓毒症小鼠细胞因子释放、肝损伤及存活的影响。
Eur Cytokine Netw. 1996 Dec;7(4):765-9.
6
Does neutrophil-mediated oxidative stress play any significant role in producing hepatocellular dysfunction during early sepsis?在早期脓毒症期间,中性粒细胞介导的氧化应激在导致肝细胞功能障碍方面是否发挥任何重要作用?
J Surg Res. 1998 Nov;80(1):75-9. doi: 10.1006/jsre.1998.5343.
7
Modulation of Kupffer cell activity: physio-pathological consequences on hepatic metabolism.库普弗细胞活性的调节:对肝脏代谢的生理病理影响
Bull Mem Acad R Med Belg. 2004;159(5-6):358-66.
8
Intravenous glycine after cecal ligation and puncture has no effect on impaired hepatic microperfusion, leukocyte adhesion, and mortality in septic rats.盲肠结扎穿孔术后静脉注射甘氨酸对脓毒症大鼠肝微灌注受损、白细胞黏附及死亡率无影响。
Microvasc Res. 2005 Jan;69(1-2):71-8. doi: 10.1016/j.mvr.2005.01.001.
9
Effect of ascorbic acid on hepatic vasoregulatory gene expression during polymicrobial sepsis.
Life Sci. 2004 Sep 3;75(16):2015-26. doi: 10.1016/j.lfs.2004.06.002.
10
Immunologic activation of hepatic macrophages in septic rats: a possible mechanism of sepsis-associated liver injury.脓毒症大鼠肝脏巨噬细胞的免疫激活:脓毒症相关肝损伤的一种可能机制。
J Lab Clin Med. 1994 Mar;123(3):430-6.