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Treatment with dimethyl fumarate ameliorates liver ischemia/reperfusion injury

World Journal of Gastroenterology 2017年第25期23卷 4508-4516页

作者： Chie Takasu Nosratola D Vaziri Shiri Li Lourdes Robles Kelly Vo Mizuki Takasu Christine Pham Seyed H Farzaneh Mitsuo Shimada Michael J Stamos Hirohito Ichii Department of Surgery Medicine University of California Departments of Surgery Institute of Health Biosciences the University of Tokushima

To investigate the hypothesis that treatment with dimethyl fumarate (DMF) may ameliorate liver ischemia/reperfusion injury (I/RI). METHODSRats were divided into 3 groups: sham, control (CTL), and DMF. DMF (25 mg/kg, twice/d) was orally administered for 2 d before the procedure. The CTL and DMF rats were subjected to ischemia for 1 h and reperfusion for 2 h. The serum alanine aminotransferase (ALT) and malondialdehyde (MDA) levels, adenosine triphosphate (ATP), NO × metabolites, anti-oxidant enzyme expression level, anti-inflammatory effect, and anti-apoptotic effect were determined. RESULTSHistological tissue damage was significantly reduced in the DMF group (Suzuki scores: sham: 0 ± 0; CTL: 9.3 ± 0.5; DMF: 2.5 ± 1.2; sham vs CTL, P < 0.0001; CTL vs DMF, P < 0.0001). This effect was associated with significantly lower serum ALT (DMF 5026 ± 2305 U/L vs CTL 10592 ± 1152 U/L, P = 0.04) and MDA (DMF 18.2 ± 1.4 μmol/L vs CTL 26.0 ± 1.0 μmol/L, P = 0.0009). DMF effectively improved the ATP content (DMF 20.3 ± 0.4 nmol/mg vs CTL 18.3 ± 0.6 nmol/mg, P = 0.02), myeloperoxidase activity (DMF 7.8 ± 0.4 mU/mL vs CTL 6.0 ± 0.5 mU/mL, P = 0.01) and level of endothelial nitric oxide synthase expression (DMF 0.38 ± 0.05-fold vs 0.17 ± 0.06-fold, P = 0.02). The higher expression levels of anti-oxidant enzymes (catalase and glutamate-cysteine ligase modifier subunit and lower levels of key inflammatory mediators (nuclear factor-kappa B and cyclooxygenase-2 were confirmed in the DMF group. CONCLUSIONDMF improved the liver function and the anti-oxidant and inflammation status following I/RI. Treatment with DMF could be a promising strategy in patients with liver I/RI.

关键词： Inflammation Reactive oxidative stress Nrf2 Ischemia dimethyl fumarate Liver

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dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse

Dimethyl fumarate inhibits antibody-induced platelet destruc...

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第十四届全国免疫学学术大会

作者： Huan Tong Yangyang Ding Xiang Gui Sixuan Zhang Jianlin Qiao Department of Hematology the Affiliated Hospital of Xuzhou Medical University

Immune thrombocytopenia(ITP) is an autoimmune disease characterized as a low platelet count resulting from immune-mediated platelet destruction. dimethyl fumarate(DMF) is widely applied for the treatment of several autoimmune diseases with immunosuppressive effect. However, whether it ameliorates ITP is unclear. This study aims to evaluate whether DMF has a preventive effect on ITP in mice. Methods: DMF(30, 60 or 90 mg/kg body weight) was intraperitoneally injected into mice followed by injection of rat anti-mouse integrin GPIIb/CD41antibody to induce ITP. Peripheral blood was isolated to measure platelet count and spleen mononuclear cells were extracted to measure Th1 and Treg cells along with detecting the levels of IFN-γ, and TGFβ-1 in plasma and CD68 expression in spleen by immuohistochemical staining. Additionally, macrophage cell line RAW264.7 was cultured and treated with DMF followed by analysis of cell apoptosis and cycle, and the expression of FcgRI, FcgRIIb and FcgRIV ***: DMF significantly inhibited antiplatelet antibody-induced platelet destruction, decreased Th1 cells and the expression of T-bet and IFN-γ, upregulated Treg cells and the expression of Foxp3 and TGF-β1 as well as reduced CD68 expression in the spleen of ITP mouse. DMF-treated RAW264.7 cells showed S-phase arrest, increased apoptosis and downregulated expression of FcgRI and FcgRIV. Meanwhile, in vitro treatment of DMF also decreased the expression of cyclin D1 and E2, reduced Bcl-2 level and increased Bax expression and caspase-3 activation. Conclusions: In conclusion, DMF prevents antibody-mediated platelet destruction in ITP mice possibly through promoting apoptosis, indicating that it might be used as a new approach for the treatment of ITP.

关键词： Immune thrombocytopenia dimethyl fumarate macrophage cell cycle apoptosis

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Monomethyl fumarate augments NK cell lysis of tumor cells through degranulation and the upregulation of NKp46 and CDIO7a

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Cellular & Molecular Immunology 2016年第1期13卷 57-64页

作者： Heidi Vego Kristin L Sand Rune A Hoglund Lars-Egil Fallang Glenn Gundersen Trygve Holmoy Azzam A Maghazachi Departmentof Physiology Institute of Medical Basic Sciences University of Oslo Oslo Norway Medical Department Biogen Idec Norway AS OsloNorway Department of Neurology Akershus University Hospital and institute of Clinical Medicine University of Oslo Oslo Norway

dimethyl fumarate （DMF） is a new drug used to treat multiple sclerosis （MS） patients. Here, we examined the effects of DMF and the DMF metabolite monomethyl fumarate （MMF） on various activities of natural killer （NK） cells. We demonstrated that MMF augments the primary CD56^＋, but not CD56^-, NK cell lysis of K562 and RAJI tumor cells. MMF induced NKp46 expression on the surface of CD56^＋, but not CD56^-, NK cells after incubation for 24 h. This effect was closely correlated with the upregulation of CD107a expression on the surface of CD56＋ NK cells and the induction of Granzyme B release from these cells through this metabolite. An anti-NKp46 antibody inhibited the MMF-induced upregulation of CD107a and the lysis of tumor cells through CD56^＋ NK cells. Thus, these results are the first to show that MMF augments CD56^＋ NK cell lysis of tumor target cells, an effect mediated through NKp46. This novel effect suggests the use of MMF for therapeutic and/or preventive protocols in cancer.

关键词： cancer prevention cancer treatment CDlO7a cytotoxicity dimethyl fumarate Granzyme B monomethyl fumarate natural killer cells NKp46

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