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TC-2559,an α4β2 nicotinic acetylcholine receptor agonist,suppresses the expression of CCL3 and IL-1β through STAT3 inhibition in cultured murine macrophages
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نویسنده
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kiguchi n. ,saika f. ,kobayashi y. ,ko m.-c. ,kishioka s.
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منبع
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journal of pharmacological sciences - 2015 - دوره : 128 - شماره : 2 - صفحه:83 -86
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چکیده
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The anti-inflammatory properties of tc-2559,an α4β2 nicotinic acetylcholine receptor (nachr) agonist,on cultured murine macrophages was investigated. tc-2559 suppressed the upregulation of cc-chemokine ligand 3 (ccl3) and interleukin-1β (il-1β) following lipopolysaccharide (lps) treatment in j774a.1 cells. tc-2559 inhibited the phosphorylation of signal transducer and activator of transcription 3 (pstat3) but not nuclear factor-κb p65 after lps. blockade of pstat3 by ag490 inhibited the upregulation of ccl3 and il-1β after lps. in conclusion,tc-2559-driven α4β2 nachr signaling suppressed the upregulation of ccl3 and il-1β by inhibiting pstat3 in inflammatory macrophages,resulting in the suppression of neuropathic pain. © 2015 the authors. production and hosting by elsevier b.v. on behalf of japanese pharmacological society. this is an open access article under the cc by-nc-nd license.
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کلیدواژه
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Chemokine; Cytokine; Nicotine
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آدرس
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department of pharmacology,wakayama medical university,811-1 kimiidera,wakayama,641-0012,japan,department of physiology and pharmacology,wake forest university school of medicine,medical center boulevard,winston-salem,nc 27157, United States, department of pharmacology,wakayama medical university,811-1 kimiidera,wakayama,641-0012, Japan, department of pharmacology,wakayama medical university,811-1 kimiidera,wakayama,641-0012, Japan, department of physiology and pharmacology,wake forest university school of medicine,medical center boulevard,winston-salem,nc 27157, United States, department of pharmacology,wakayama medical university,811-1 kimiidera,wakayama,641-0012, Japan
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Authors
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