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- Kawabata Atsufumi
- Division of Pharmacology and Pathophysiology, School of Pharmacy, Kinki University
書誌事項
- タイトル別名
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- Prostaglandin E2 and Pain-An Update
この論文をさがす
説明
Prostaglandin E2 (PGE2), a cyclooxygenase (COX) product, is the best known lipid mediator that contributes to inflammatory pain. Nonsteroidal anti-inflammatory drugs (NSAIDs), inhibitors of COX-1 and/or COX-2, suppress inflammatory pain by reducing generation of prostanoids, mainly PGE2, while they exhibit gastrointestinal, renal and cardiovascular toxicities. Selective inhibitors of microsomal PGE synthase-1 and subtype-selective antagonists of PGE2 receptors, particularly EP1 and EP4, may be useful as analgesics with minimized side-effects. Protein kinase C (PKC) and PKA downstream of EP1 and EP4, respectively, sensitize/activate multiple molecules including transient receptor potential vanilloid-1 (TRPV1) channels, purinergic P2X3 receptors, and voltage-gated calcium or sodium channels in nociceptors, leading to hyperalgesia. PGE2 is also implicated in neuropathic and visceral pain and in migraine. Thus, PGE2 has a great impact on pain signals, and pharmacological intervention in upstream and downstream signals of PGE2 may serve as novel therapeutic strategies for the treatment of intractable pain.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 34 (8), 1170-1173, 2011
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204632583424
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- NII論文ID
- 40018913999
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 11174210
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- PubMed
- 21804201
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可