2015
DOI: 10.1016/j.intimp.2015.03.015
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Irbesartan attenuates production of high-mobility group box 1 in response to lipopolysaccharide via downregulation of interferon-β production

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Cited by 4 publications
(3 citation statements)
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References 33 publications
(35 reference statements)
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“…Irbesartan exerts a neuroprotective effect by inhibiting the activation of microglia and macrophages [132]. This medicament reduces the production of IFN-beta and the expression of iNOS, and thus inhibiting NO production [133]. Irbesartan also inhibits the expression of MCP-1 mRNA in THP-1 monocyte cell line stimulated with TNF-α and activates PPARγ [134].…”
Section: Candesartan Irbesartanmentioning
confidence: 99%
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“…Irbesartan exerts a neuroprotective effect by inhibiting the activation of microglia and macrophages [132]. This medicament reduces the production of IFN-beta and the expression of iNOS, and thus inhibiting NO production [133]. Irbesartan also inhibits the expression of MCP-1 mRNA in THP-1 monocyte cell line stimulated with TNF-α and activates PPARγ [134].…”
Section: Candesartan Irbesartanmentioning
confidence: 99%
“…the general number of immune cells in bronchoalveolar lavage fluid [125]; -the release of Th2-lymphocyte (IL-4, IL-5 and IL-13) and Th1-lymphocyte (IL-2 and IFN-γ) cytokines [125]; -inhibiting the activation of microglia and macrophages [132]; -the production of IFN-beta and the expression of iNOS, and thus inhibits NO production [133]; -expression of MCP-1 mRNA in THP-1 monocyte cell line stimulated with TNF-α and activates PPARγ [134]; -macrophage infiltration [136].…”
Section: Reduction Inmentioning
confidence: 99%
“…22,23) Furthermore, in vitro, the expression levels of HMGB1 are reduced by inhibiting AT1 receptor activation following stimulation with lipopolysaccharide. 24) The aforementioned findings, along with the fact that Ang II is increased under PO 2 and that HMGB1 expression is enhanced by mechanical stress in cultured cardiac myocytes, 16) led to the hypothesis that Ang II may regulate the expression and release of HMGB1 in hearts under PO through AT1 and AT2 receptor signaling. The present study explored this hypothesis by blocking Ang II receptors in transverse aortic constriction (TAC)-induced hypertrophic mice in vivo and in cardiac myocytes treated with Ang II in vitro.…”
mentioning
confidence: 99%