Item type |
デフォルトアイテムタイプ_(フル)(1) |
公開日 |
2023-03-18 |
タイトル |
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タイトル |
The long-term exposure of rat cultured dorsal root ganglion cells to bradykinin induced the release of prostaglandin E2 by the activation of cyclooxygenase-2 |
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言語 |
en |
作成者 |
Inoue, Atsuko
Iwasa, Mikiko
Nishikura, Yumi
Ogawa, Shinya
Nakasuka, Ayaka
Nakata, Yoshihiro
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利情報 |
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権利情報 |
Copyright (c) 2006 Elsevier Ltd. |
主題 |
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主題Scheme |
Other |
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主題 |
B2 receptor |
主題 |
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主題Scheme |
Other |
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主題 |
Bradykinin |
主題 |
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主題Scheme |
Other |
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主題 |
Cyclooxygenase-2 |
主題 |
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主題Scheme |
Other |
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主題 |
Prostaglandin E2 |
主題 |
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主題Scheme |
Other |
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主題 |
Rat dorsal root ganglion cells |
主題 |
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主題Scheme |
NDC |
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主題 |
490 |
内容記述 |
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内容記述 |
The effects of long-term exposure of primary cultured rat dorsal root ganglion (DRG) cells to bradykinin (BK), compared to short-term exposure, were investigated to establish whether BK could induce prostaglandin E2 (PGE2) release from DRG cells. Short-term exposure (30 min) resulted in a small but significant amount of PGE2 release which was mainly inhibited by a selective COX-1 inhibitor, SC-560 but only partially by a selective COX-2 inhibitor, NS-398, and did not induce COX-2 protein as determined by Western blotting. In contrast, long-term exposure (3 hr) induced a large amount of PGE2 release, which was completely abolished by indomethacin or NS-398. The level of COX-2 mRNA began to be detected by ribonuclease protection assay after 30 min of 100 nM BK exposure, maintained maximal expression for 1 h, and subsequently declined to the basal level. The level of COX-2 protein was expressed to follow the time course of COX-2 mRNA induction by BK in a delayed but similar kinetic manner. The expression of COX-2 induced by BK in DRG cells was inhibited by a BK B2 receptor antagonist, HOE140, but not a B1 receptor antagonist, Lys-des-Arg9, (Leu8)-BK. Thus BK has been shown to induce COX-2 protein by B2 receptor, which may cause prostanoid generation in rat DRG cells, which may play an important role in the pathogenesis of inflammatory pain and hyperalgesia around the primary sensory neurons. |
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言語 |
en |
出版者 |
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出版者 |
Elsevier |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
出版タイプ |
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出版タイプ |
AO |
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出版タイプResource |
http://purl.org/coar/version/c_b1a7d7d4d402bcce |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
10.1016/j.neulet.2006.03.026 |
関連情報 |
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識別子タイプ |
PMID |
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関連識別子 |
16580130 |
関連情報 |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
http://dx.doi.org/10.1016/j.neulet.2006.03.026 |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
0304-3940 |
収録物識別子 |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00754925 |
開始ページ |
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開始ページ |
242 |
書誌情報 |
Neuroscience Letters
Neuroscience Letters
巻 401,
号 3,
p. 242-247,
発行日 2006-07-03
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旧ID |
17112 |