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Int. J. Mol. Sci. 2014, 15(8), 13223-13235; doi:10.3390/ijms150813223

Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes

1
Department of Psychiatry, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80761, Taiwan
2
Department of Pediatrics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80761, Taiwan
3
Department of Psychiatry, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80761, Taiwan
4
Institute of Biomedical Science, National Sun Yat-Sen University, Kaohsiung 80424, Taiwan
5
Department of Community Psychiatry, Kai-Suan Psychiatric Hospital, 130 Kai-Suan 2nd Road, Kaohsiung 80276, Taiwan
6
Department of Pediatrics, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung 81267, Taiwan
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 1 April 2014 / Revised: 12 June 2014 / Accepted: 7 July 2014 / Published: 28 July 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Major depressive disorder and cardiovascular disease are common serious illnesses worldwide. Selective serotonin reuptake inhibitors and norepinephrine-dopamine reuptake inhibitors may reduce the mortality of cardiovascular disease patients with comorbid depression. Interferon-γ-inducible protein 10 (IP-10), a type 1 T helper cell (Th1)-related chemokine, contributes to manifestations of atherosclerosis during cardiovascular inflammations; however, the pathophysiological mechanisms linking cardiovascular disease and effective antidepressants have remained elusive. We investigated the in vitro effects of six different classes of antidepressants on the IP-10 chemokine expression in lipopolysaccharide (LPS)-stimulated monocytes, and their detailed intracellular mechanisms. The human monocytes were pretreated with antidepressants (10−8–10−5 M) before LPS-stimulation. IP-10 was measured by enzyme-linked immunosorbent assay (ELISA) and then intracellular signaling was investigated using Western blotting and chromatin immunoprecipitation. Fluoxetine and bupropion suppressed LPS-induced IP-10 expression in monocytes, and they had no cytotoxic effects. Furthermore, fluoxetine inhibited LPS-induced IP-10 expression via the mitogen-activated protein kinase (MAPK)-p38 pathway. Fluoxetine and bupropion could not only treat depression but also reduce Th1-related chemokine IP-10 production in human monocytes. Our results may indicate a possible mechanism related to how particular antidepressants reduce the risk of cardiovascular disease. View Full-Text
Keywords: antidepressants; IP-10; chemokine; monocyte; LPS antidepressants; IP-10; chemokine; monocyte; LPS
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MDPI and ACS Style

Tsai, J.-H.; Kuo, C.-H.; Yang, P.; Cheng, K.-H.; Wang, P.-W.; Chen, C.-C.; Hung, C.-H. Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes. Int. J. Mol. Sci. 2014, 15, 13223-13235.

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