In vitro inhibitory effects of cirsiliol on IL-6-induced STAT3 activation through anti-inflammatory activity |
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| Institution: | 1. Immunoregulatory Materials Research Center, Korea Research Institute of Bioscience and Biotechnology, 181 Ipsin-gil, Jeongeup-si, Jeonbuk 56212, Republic of Korea;2. Department of Molecular Biology, Chonbuk National University, Jeonju 54896, Republic of Korea;3. Department of Marine Bio Food Science, College of Fisheries and Ocean Science, Chonnam National University, Yeosu 59626, Republic of Korea;1. Department of Physiology and Developmental Biology, Brigham Young University, 4005 LSB, Provo, UT 84602, USA;2. Frost Biologic, Inc., 5201 South Green St., Suite 160, Salt Lake City, UT 84123, USA;1. Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, PO Box 2457, Riyadh 11451, Saudi Arabia;2. Department of Chemistry, College of Science and Humanities, Prince Sattam bin Abdulaziz University, PO Box 83, Al Kharj 11942, Saudi Arabia;3. Chemistry of Natural Products Group, Centre of Excellence for Advanced Sciences, National Research Centre, 33 El-Bohouth St. (Former El-Tahrir St.) Dokki, Cairo 12622, Egypt;1. Facultad de Ciencias Naturales e IML, Universidad Nacional de Tucumán, Argentina;2. Instituto de Bioprospección y Fisiología Vegetal (INBIOFIV), CONICET-UNT, San Miguel de Tucumán, Tucumán, Argentina;3. Instituto de Bionanotecnología del NOA (INBIONATEC), CONICET-UNSE, Santiago del Estero, Argentina |
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| Abstract: | Many studies have identified and described various medicinal effects of cirsiliol. Here, we investigated the signaling pathway involved in the anti-inflammatory effects of cirsiliol on IL-6-induced activity. Cirsiliol showed no cytotoxicity and inhibited pSTAT3-induced luciferase activity. At the molecular level, cirsiliol suppressed the expression of IL-6-induced inflammatory marker genes such as CRP, IL-1β, ICAM-1 and SOCS3, IL-6-induced activation of Jak2, gp130, STAT3 and ERK and nuclear translocation of STAT3, as measured by PCR, immunofluorescence staining and western blot analysis. However, the interaction between IL-6 and its receptor was not affected by cirsiliol treatment. These results indicate that cirsiliol attenuates IL-6-induced cellular signaling by regulating Jak2 phosphorylation. Therefore, cirsiliol could be a therapeutic agent for IL-6-related inflammatory diseases. |
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| Keywords: | Cirsiliol Inflammation IL-6 STAT3 Jak2 |
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