S H Lee1, J Y Kim, G S Seo, Y-C Kim, D H Sohn. 1. Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Abstract
OBJECTIVES: 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. METHODS: 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-1beta (IL-1beta) 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. RESULTS: ISL markedly suppressed LPS-induced NO, IL-1beta, 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. CONCLUSIONS: ISL is an effective HO-1 inducer capable of inhibiting macrophage-derived inflammation.
OBJECTIVES: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. METHODS: 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-1beta (IL-1beta) and tumornecrosis 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. RESULTS:ISL markedly suppressed LPS-induced NO, IL-1beta, 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. CONCLUSIONS:ISL is an effective HO-1 inducer capable of inhibiting macrophage-derived inflammation.