Abstract:
:It has been suggested that the supernatant of LPSstimulated macrophages (macrophage nociceptive factor, MNF) promotes nociception in mice. Intraperitoneal administration of MNF induced dose-related writhing, which reached a plateau between 18 and 26 min after injection and decreased within 60 min. The release of MNF was inhibited by the pretreatment of the macrophages with cycloheximide, a protein synthesis inhibitor, or with the glucocorticoid dexamethasone. Cyclooxygenase inhibitors, such as indomethacin or paracetamol, had no effect. The MNF-induced nociception was inhibited in a dose-related manner by pretreatment of the animals with indomethacin, paracetamol or dexamethasone. Pretreatment of the animals with the sympatholytics guanethidine and atenolol partially reduced the MNF nociception, which was abolished by the combination of guanethidine or atenolol with indomethacin. The preincubation of MNF with antisera against TNF-alpha, IL-1 or IL-8 partially inhibited its nociceptive effect. Intraperitoneal injection of a mixture of the recombinants cytokines TNF-alpha, IL-1 and IL-8 mimicked MNF nociception. The individual injection of these cytokines was unable to induce the nociceptive effect. In conclusion, our data suggest that the nociceptive activity of the supernatant of LPSstimulated macrophages is explained by the presence of TNF-alpha, IL-1 and IL-8, the nociceptive activity of which (in mice) seems to be due to the release of cyclooxygenase and sympathetic metabolites.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Thomazzi SM,Ribeiro RA,Campos DI,Cunha FQ,Ferreira SHdoi
10.1080/09629359791686subject
Has Abstractpub_date
1997-01-01 00:00:00pages
195-200issue
3eissn
0962-9351issn
1466-1861journal_volume
6pub_type
杂志文章abstract::The increased morbidity, mortality, and ineffective treatment associated with the pathogenesis of chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD) have generated much research interest. The key role is played by phospholipases from the A2 superfamily: enzymes which are invo...
journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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abstract:BACKGROUND:Icariin (ICA) is an active compound extracted from Epimedium brevicornum Maxim. Previous reports have shown that icariin has a clinically significant therapeutic effect on rheumatoid arthritis. However, little is known about the mechanism by which icariin inhibits cartilage and bone degradation. METHODS:New...
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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更新日期:2012-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2013/979748
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journal_title:Mediators of inflammation
pub_type: 杂志文章
doi:10.1155/2013/736085
更新日期:2013-01-01 00:00:00
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journal_title:Mediators of inflammation
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doi:10.1155/MI/2006/31919
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
pub_type: 临床试验,杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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更新日期:2007-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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更新日期:1995-01-01 00:00:00
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journal_title:Mediators of inflammation
pub_type: 杂志文章,评审
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章,meta分析
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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journal_title:Mediators of inflammation
pub_type: 杂志文章
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更新日期:2020-08-04 00:00:00
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journal_title:Mediators of inflammation
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