Journal
INFLAMMATION RESEARCH
Volume 58, Issue 5, Pages 257-262Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-008-8183-6
Keywords
Isoliquiritigenin; Nitric oxide; Tumor necrosis factor-alpha; Heme oxygenase-1; Extracellular signal-regulated kinase1/2
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Funding
- Ministry of Commerce Industry and Energy (MOCIE) [RTI05-03-02]
- Ministry of Knowledge Economy (MKE), Republic of Korea [B0008476] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [핵C6A3403] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Isoliquiritigenin (ISL), one of the major constituents of Dalbergia odorifera T. Chen (Leguminosae), is reported to exert anti-inflammatory effects, but the relevant anti-inflammatory mechanisms are not completely understood. Heme oxygenase-1 (HO-1) has been proven to be involved in the resolution of inflammatory responses. In this study, we investigated whether ISL could induce HO-1 expression in RAW264.7 macrophages, and if so, whether HO-1 could mediate the anti-inflammatory effects of ISL. The protein expression of inducible nitric oxide synthase and HO-1 was analyzed by western blot analysis. The production of nitric oxide (NO) and interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) was assayed by Griess and ELISA, respectively. The TNF-alpha and HO-1 mRNA expression was analyzed by northern blot analysis. ISL markedly suppressed LPS-induced NO, IL-1 beta, and TNF-alpha production. ISL induced HO-1 expression through the extracellular signal-regulated kinase1/2 pathway in RAW264.7 macrophages. The effects of ISL on LPS-induced NO and TNF-alpha production were reversed by the HO-1 inhibitor, tin protoporphyrin. ISL is an effective HO-1 inducer capable of inhibiting macrophage-derived inflammation.
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