Induction of microsomal prostaglandin E synthase-1 contributes to neuroinflammation and neurological dysfunctions in a mouse intracerebral hemorrhage model.
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- Ikeda-Matsuo Yuri
- Dev. Pharmacol., Dept. Clin. Pham., Fac. Pharmac. Sci., Hokuriku Univ.
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- Miyahara Nobutaka
- Dev. Pharmacol., Dept. Clin. Pham., Fac. Pharmac. Sci., Hokuriku Univ.
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- Yozawa Chika
- Lab. Pharmacol., Sch. Pharmac. Sci., Kitasato Univ.
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- Kawano Saki
- Lab. Pharmacol., Sch. Pharmac. Sci., Kitasato Univ.
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- Mizuguchi Aika
- Lab. Pharmacol., Sch. Pharmac. Sci., Kitasato Univ.
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- Naito Yasuhito
- Lab. Pharmacol., Sch. Pharmac. Sci., Kitasato Univ.
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- Uematsu Satoshi
- Dept. Immunol. Genomic, Osaka City Univ. Grad. Sch. Med.
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- Akira Shizuo
- Lab. Host Defense, WPI Immunol. Front. Res. Ctr., Osaka Univ.
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- Takahashi Tatsuo
- Dev. Pharmacol., Dept. Clin. Pham., Fac. Pharmac. Sci., Hokuriku Univ.
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- Tanabe Mitsuo
- Lab. Pharmacol., Sch. Pharmac. Sci., Kitasato Univ.
Bibliographic Information
- Other Title
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- プロスタグランジンE合成酵素-1の誘導はマウス脳出血モデルにおける神経炎症と神経学的運動障害に寄与する
Abstract
<p>We have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for PGE2 synthesis, is a critical factor of stroke-reperfusion injury. In this study, we investigated the role of mPGES-1 in neuroinflammation and neurological dysfunctions observed after intracerebral hemorrhage (ICH). Collagenase was injected into the left striatum of adult mPGES-1 knockout (KO) and wild-type (WT) mice. In WT mice, mRNA and protein of mPGES-1 were significantly up-regulated in striatum and cerebral cortex after ICH. In mPGES-1 KO mice, although the hemorrhage and edema size were almost the same as WT mice, survival rate was significantly higher than WT mice. The PGE2 production, TNF-α induction and glial activation after ICH in mPGES-1 KO brain were significantly less than those in WT brain. DAPI and TUNEL staining showed ICH-induced nuclear condensation and DNA fragmentation in mPGES-1 KO striatum were less than those in WT striatum. Furthermore, mPGES-1 KO mice showed better performance in stepping error test, rotarod test and neurological dysfunction scoring compared with the WT mice. These results suggest that mPGES-1 contributes to ICH-induced neuroinflammation, neuronal apoptosis, neurological dysfunctions and mortality through PGE2 production. Thus, mPGES-1 may be a new therapeutic target for ICH.</p>
Journal
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- Proceedings for Annual Meeting of The Japanese Pharmacological Society
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Proceedings for Annual Meeting of The Japanese Pharmacological Society 93 (0), 3-O-084-, 2020
Japanese Pharmacological Society
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Keywords
Details 詳細情報について
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- CRID
- 1390002184882606208
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- NII Article ID
- 130007811789
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- ISSN
- 24354953
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed