Induction of heme oxygenase-1 mediates the anti-inflammatory effects of the ethanol extract of Rubus coreanus in murine macrophages

Park, Junhong; Oh, Sun-mee; Lim, Soon Sung; Lee, Yeon Sil; Shin, Hyun‐Kyung; Oh, Yang-Seok; Choe, Nonghoon; Park, Jung Han Yoon; Kim, Jin‐Kyung

doi:10.1016/j.bbrc.2006.10.008

Cited by 51 publications

(28 citation statements)

References 25 publications

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“…An appropriate and proper inflammatory response depends on the careful regulation of a number of mediators such as cytokines, which are secreted by inflammatory cells such as macrophages and neutrophils (Park et al, 2006;Zhou et al, 2007). Macrophages are known to play a pivotal role in the host's defense against harmful materials and are involved in a variety of diseases including autoimmune diseases, pathogenic infections, and inflammatory disorders (Dokka et al, 2001;Kang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

Yang

Moon

Kim

et al. 2010

J. Zhejiang Univ. Sci. B

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Seaweed has been used in traditional cosmetics and as a herbal medicine in treatments for cough, boils, goiters, stomach ailments, and urinary diseases, and for reducing the incidence of tumors, ulcers, and headaches. Despite the fact that seaweeds are frequently used in the practice of human health, little is known about the role of seaweed in the context of inflammation. This study aimed to investigate the influence of Jeju endemic seaweed on a mouse macrophage cell line (RAW 264.7) under the stimulation of lipopolysaccharide (LPS). Ethyl acetate extracts obtained from 14 different kinds of Jeju seaweeds were screened for inhibitory effects on pro-inflammatory mediators. Our results revealed that extracts from five seaweeds, Laurencia okamurae, Grateloupia elliptica, Sargassum thunbergii, Gloiopeltis furcata, and Hizikia fusiformis, were potent inhibitors of the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E 2 (PGE 2 ), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). Based on these results, the anti-inflammatory effects and low cell toxicity of these seaweed extracts suggest potential therapeutic applications in the regulation of the inflammatory response.

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Section: Introductionmentioning

confidence: 99%

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

Yang

Moon

Kim

et al. 2010

J. Zhejiang Univ. Sci. B

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“…Therefore, blocking excessive nitric oxide production through inhibiting iNOS expression may improve abnormal inflammatory responses. iNOS expression is regulated by nuclear factor jB (NF-jB) and mitogen-activated protein kinase (MAPK) pathways [6][7][8].Haem oxygenase 1 (HO-1) has anti-inflammatory properties associated with cytoprotective responses [9,10]. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is critical for HO-1 induction and is activated by diverse oxidants, pro-oxidants, antioxidants and chemopreventive agents [11,12].…”

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confidence: 99%

2′‐Methoxy‐4′6′‐Bis(Methoxymethoxy)Chalcone Inhibits Nitric Oxide Production in Lipopolysaccharide‐Stimulated RAW 264.7 Macrophages

Jin

Lee

Park

et al. 2010

Basic Clin Pharma Tox

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Chalcones have anti-inflammatory properties. Here, we synthesized 2¢-methoxy-4¢6¢-bis(methoxymethoxy)chalcone (MBMC) and examined its anti-inflammatory effects. MBMC inhibited nitric oxide production and inducible nitric oxide synthase (iNOS) expression in lipopolysaccharide (LPS)-stimulated RAW 264.7 murine macrophages. MBMC also blocked LPSinduced activation of nuclear factor jB (NF-jB), p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK). MBMC increased haem oxygenase 1 (HO-1) expression and nuclear accumulation of nuclear factor-erythroid 2-related factor 2 (Nrf2), an essential transcription factor for HO-1 induction. Treatment with tin protoporphyrin, a selective inhibitor of HO-1, reversed the inhibition of nitric oxide production by MBMC, suggesting that HO-1 induction mediates MBMC-mediated suppression of nitric oxide production. MBMC treatment rapidly and transiently decreased glutathione (GSH) levels, and treatment with GSH-Et (cell permeable form of GSH) or N-acetylcysteine (precursor of GSH) counteracted the HO-1 and Nrf2 expression elicited by MBMC, indicating that MBMC-induced HO-1 expression requires transient depletion of GSH. In summary, MBMC inhibits LPS-stimulated nitric oxide production via down-regulation of inflammatory pathways (NF-jB, p38 and JNK) and induction of the protective enzyme, HO-1.Nitric oxide, a bioactive free radical, regulates many physiological processes [1]. However, excessive nitric oxide production is implicated in the pathogenesis of various inflammatory diseases, such as haemorrhagic and septic shock, chronic infections and rheumatoid arthritis [2][3][4]. Inducible nitric oxide synthase (iNOS) is induced in response to inflammatory stimuli and catalyses the production of large amounts of nitric oxide during inflammation [5]. Therefore, blocking excessive nitric oxide production through inhibiting iNOS expression may improve abnormal inflammatory responses. iNOS expression is regulated by nuclear factor jB (NF-jB) and mitogen-activated protein kinase (MAPK) pathways [6][7][8].Haem oxygenase 1 (HO-1) has anti-inflammatory properties associated with cytoprotective responses [9,10]. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is critical for HO-1 induction and is activated by diverse oxidants, pro-oxidants, antioxidants and chemopreventive agents [11,12]. Activated Nrf2 accumulates in the nucleus, binds to the antioxidant response element and up-regulates antioxidant enzymes, including HO-1 [13]. The nuclear accumulation of Nrf2 can be regulated by translocation from the cytosol and ⁄ or by increased expression level of Nrf2 [14]. Glutathione (GSH) is an antioxidant that protects cells from oxidative and nitrosative stress [15]. Depletion of intracellular GSH may induce Nrf2 expression as a cellular defence mechanism to increase GSH content [16]. It has been shown that depletion of GSH induces HO-1 expression and inhibits nitric oxide production [17].We have previously demonstrated that 2¢,4¢,6¢-tris(methoxymethoxy)chalcone (TMMC), a syn...

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“…Several drugs and plant extracts have been reported to modify NO production by murine macrophages (25)(26)(27)(28). Herein, 6-CMMP exhibited this property at all concentrations and it performed significantly in a dose-dependent manner when macrophages were activated by IFN-c, showing pronounced effects at 500 lM.…”

Section: Discussionmentioning

confidence: 80%

Modulatory Effects of 6‐Carboxymethylthiopurine on Activated Murine Macrophages

et al. 2008

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The immunological activity of macrophages against pathogens in hosts includes the phagocytosis and the production of nitric oxide. We report herein the investigation of the effect of 6‐carboxymethylthiopurine on nitric oxide production by murine macrophages as well as its effect on the cell viability and proliferation after stimulus with Mycobacterium bovis bacille Calmette–Guérin, interferon‐gamma or a combination of both. J774A.1 macrophages stimulated or not by bacille Calmette–Guérin (20 μg/mL), interferon‐gamma or both, were cultured in the presence of 6‐carboxymethylthiopurine (125, 250 and 500 μm). Nitric oxide production was measured by the Griess method and cell viability/proliferation by the diphenyltetrazolium assay [3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide]. We observed an increase of J774A.1 cell proliferation after stimulus with bacille Calmette–Guérin at 125, 250 and 500 μm (69.1, 124.0 and 89.7%, respectively) and with interferon‐gamma at 125 and 250 μm (64.8% and 61.7%, respectively) (p < 0.05). In all cultures treated with 6‐carboxymethylthiopurine, interferon‐gamma‐activated nitric oxide production by J774A.1 cells decreased as well as when subjected to interferon‐gamma plus bacille Calmette–Guérin stimuli at 500 μm (p < 0.05). Altogether these data point to an anti‐inflammatory effect of 6‐carboxymethylthiopurine on stimulated macrophages.

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Induction of heme oxygenase-1 mediates the anti-inflammatory effects of the ethanol extract of Rubus coreanus in murine macrophages

Cited by 51 publications

References 25 publications

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

Inhibitory effect of Jeju endemic seaweeds on the production of pro-inflammatory mediators in mouse macrophage cell line RAW 264.7

2′‐Methoxy‐4′6′‐Bis(Methoxymethoxy)Chalcone Inhibits Nitric Oxide Production in Lipopolysaccharide‐Stimulated RAW 264.7 Macrophages

Modulatory Effects of 6‐Carboxymethylthiopurine on Activated Murine Macrophages

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