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本文引用的文献

1
Differential cardiopulmonary recruitment of neutrophils during hemorrhagic shock: a role for ICAM-1?失血性休克期间中性粒细胞在心肺的差异性募集：细胞间黏附分子-1的作用？
Shock. 2001 Dec;16(6):444-8. doi: 10.1097/00024382-200116060-00007.
2
"Haemoxygenase-1 induction and exhaled markers of oxidative stress in lung diseases", summary of the ERS Research Seminar in Budapest, Hungary, September, 1999.“血红素加氧酶-1的诱导作用与肺部疾病中氧化应激的呼出标记物”，1999年9月于匈牙利布达佩斯举行的欧洲呼吸学会研究研讨会综述
Eur Respir J. 2001 Aug;18(2):420-30. doi: 10.1183/09031936.01.00231201.
3
Carbon monoxide from heme catabolism protects against hepatobiliary dysfunction in endotoxin-treated rat liver.血红素分解代谢产生的一氧化碳可保护内毒素处理的大鼠肝脏免受肝胆功能障碍的影响。
Gastroenterology. 2001 Apr;120(5):1227-40. doi: 10.1053/gast.2001.23249.
4
Differential effects of a Toll-like receptor antagonist on Mycobacterium tuberculosis-induced macrophage responses.Toll样受体拮抗剂对结核分枝杆菌诱导的巨噬细胞反应的不同影响。
J Immunol. 2001 Mar 15;166(6):4074-82. doi: 10.4049/jimmunol.166.6.4074.
5
Heme oxygenase: colors of defense against cellular stress.血红素加氧酶：抵御细胞应激的防护色彩
Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1029-37. doi: 10.1152/ajplung.2000.279.6.L1029.
6
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Biochem Pharmacol. 2000 Jul 15;60(2):275-83. doi: 10.1016/s0006-2952(00)00324-5.
7
Inhibition of lipopolysaccharide-induced signal transduction in endotoxin-tolerized mouse macrophages: dysregulation of cytokine, chemokine, and toll-like receptor 2 and 4 gene expression.脂多糖诱导的内毒素耐受小鼠巨噬细胞信号转导的抑制：细胞因子、趋化因子以及Toll样受体2和4基因表达的失调
J Immunol. 2000 Jun 1;164(11):5564-74. doi: 10.4049/jimmunol.164.11.5564.
8
The biology of Toll-like receptors.Toll样受体的生物学
Cytokine Growth Factor Rev. 2000 Sep;11(3):219-32. doi: 10.1016/s1359-6101(00)00006-x.
9
Transcriptional activation of heme oxygenase-1 gene in mouse spleen, liver and kidney cells after treatment with lipopolysaccharide or hemoglobin.用脂多糖或血红蛋白处理后小鼠脾脏、肝脏和肾脏细胞中血红素加氧酶-1基因的转录激活
Cell Biol Int. 1999;23(7):465-74. doi: 10.1006/cbir.1999.0375.
10
Mouse toll-like receptor 4.MD-2 complex mediates lipopolysaccharide-mimetic signal transduction by Taxol.小鼠Toll样受体4-MD-2复合物介导紫杉醇的脂多糖模拟信号转导。
J Biol Chem. 2000 Jan 28;275(4):2251-4. doi: 10.1074/jbc.275.4.2251.

Toll样受体4介导脂多糖诱导的小鼠肝脏血红素加氧酶-1表达：肿瘤坏死因子-α和白细胞介素-1β的作用

TLR4 mediates LPS-induced HO-1 expression in mouse liver: role of TNF-alpha and IL-1beta.

作者信息

Song Yong, Shi Yi, Ao Li-Hua, Harken Alden H, Meng Xian-Zhong

机构信息

Department of Respiratory Diseases, Nanjing Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, Jiangsu Province, China.

出版信息

World J Gastroenterol. 2003 Aug;9(8):1799-803. doi: 10.3748/wjg.v9.i8.1799.

DOI:10.3748/wjg.v9.i8.1799
PMID:12918124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4611547/
Abstract

AIM

Heme oxygenase (HO)-1 catalyzes the conversion of heme to biliverdin, iron and carbon monoxide. HO-1 is induced by many stimuli including heme, Hb, heat stress,lipopolysaccharide (LPS) and cytokines. Previous studies demonstrated that LPS induced HO-1 gene activation and HO-1 expression in liver. However, the mechanisms of LPS-induced HO-1 expression in liver remain unknown. The effect of toll-like receptor-4 (TLR4) on LPS-induced liver HO-1 expression and the role of TNF-alpha and IL-1beta in this condition were determined.

METHODS

HO-1 expression was determined by immunofluorescent staining and immunoblotting. Double immunofluorescent staining was performed to determine the cell type of HO-1 expression in liver.

RESULTS

A low dose of LPS significantly increased HO-1 expression in the liver which was localized in Kupffer cells only. Furthermore, HO-1 expression was enhanced by three doses of LPS. HO-1 expression was significantly inhibited in the liver of TLR4 mutant mice. While the liver HO-1 expression in TNF KO mice was much lower than that in C57 mice following the same LPS treatment, IL-1beta KO had a slight influence on liver HO-1 expression following LPS treatment.

CONCLUSION

The present results confirm that macrophages are the major source of HO-1 in the liver induced by LPS. This study demonstrates that TLR4 plays a dominant role in mediating HO-1 expression following LPS. LPS-induced HO-1 expression is mainly mediated by endogenous TNF-alpha, but only partially by endogenous IL-1beta.

摘要

目的

血红素加氧酶（HO）-1催化血红素转化为胆绿素、铁和一氧化碳。HO-1可被多种刺激诱导，包括血红素、血红蛋白、热应激、脂多糖（LPS）和细胞因子。先前的研究表明，LPS可诱导肝脏中HO-1基因激活和HO-1表达。然而，LPS诱导肝脏中HO-1表达的机制仍不清楚。本研究确定了Toll样受体4（TLR4）对LPS诱导的肝脏HO-1表达的影响以及肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）在此过程中的作用。

方法

通过免疫荧光染色和免疫印迹法检测HO-1表达。采用双重免疫荧光染色法确定肝脏中HO-1表达的细胞类型。

结果

低剂量LPS可显著增加肝脏中HO-1的表达，且仅定位于库普弗细胞。此外，三种剂量的LPS均可增强HO-1表达。在TLR4突变小鼠的肝脏中，HO-1表达显著受到抑制。相同LPS处理后，TNF基因敲除（KO）小鼠肝脏中的HO-1表达远低于C57小鼠，而IL-1β KO小鼠在LPS处理后肝脏HO-1表达受到轻微影响。

结论

本研究结果证实巨噬细胞是LPS诱导肝脏中HO-1的主要来源。本研究表明，TLR4在介导LPS诱导的HO-1表达中起主导作用。LPS诱导的HO-1表达主要由内源性TNF-α介导，但仅部分由内源性IL-1β介导。