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CORM-2 inhibits intracerebral hemorrhage-mediated inflammation

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机构: [a]Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China [b]Advanced Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China [c]Department of China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China [d]Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, China [e]Department of Neurology, Jingdezhen First People’s Hospital, Jingdezhen, China [f]Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, Shanghai, China [g]Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA [h]Department of Neurosurgery, Henry Ford Health System, Detroit, MI, USA
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关键词: Intracerebral hemorrhage carbon monoxide releasing molecule-2 IKK/NF-kappa B signal pathway

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Background and purpose: Low-dose of carbon monoxide delivered by CO-releasing molecule-2 (CORM-2) had been confirmed having anti-inflammatory efficacy in some inflammatory diseases. Herein, we assessed the usefulness of CORM-2 in correcting intracerebral hemorrhage (ICH)-mediated inflammation. Methods: Healthy male Sprague Dawley (SD) rats randomly entered into four groups: sham-ICH, ICH, ICH+CORM-2, and ICH+ inactive carbon monoxide releasing molecule 2 (iCORM-2). ICH was induced by 50 mu l of autologous arterial blood injected in situ in the rat brain. Neuro-functions of the ICH rats were evaluated with Garcia 18 scores at the 6th, 24th , 48th hou, and the fifthh day post-ICH. And brain tissues surrounding the hematoma area were collected from all ICH rats and assayed with Western blot and immunofluoresence analysis. Results: Neuro-dysfunctions in ICH rats were very severe than those in ICH +CORM-2 rats. Compared to sham group, the levels of HO-1, IKK beta, NF-kappa B, and TNF-alpha in ICH group began to elevate at the 6th hour, and reached to peak at the 48th hour post-ICH, all p < 0.05. While in ICH +CORM-2 group, the expressions of IKK beta, NF-kappa B, and TNF-alpha were very weaker than that in ICH group at every time points mentioned above; however, this phenomenon was not reproduced in ICH + iCORM-2 group. HO-1 in ICH+CORM-2 group highlighted in perihematomal area with many activated microglia (Iba-1-positive cells) and co-expressed with TNF-alpha, all of which were diminished at the fifth day post-ICH. Conclusion: CORM-2 may attenuate ICH-mediated inflammation by inhibiting microglial activation, which may involve the IKK/NF-kappa B pathway.

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出版当年[2020]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
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出版当年[2019]版:
Q3 CLINICAL NEUROLOGY Q3 NEUROSCIENCES
最新[2023]版:
Q3 CLINICAL NEUROLOGY Q4 NEUROSCIENCES

影响因子: 最新[2023版] 最新五年平均 出版当年[2019版] 出版当年五年平均 出版前一年[2018版] 出版后一年[2020版]

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第一作者机构: [a]Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China [b]Advanced Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China [c]Department of China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China [d]Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, China
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通讯机构: [a]Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China [b]Advanced Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China [c]Department of China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China [d]Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, China [*1]Xuanwu Hospital, Capital Medical University, Beijing 100053, China [*2]Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi 332000, China
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