Suppression by Azelastine Hydrochloride of NF-κB Activation Involved in Generation of Cytokines and Nitric Oxide
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- Yoneda Kazunori
- Department of Oral Surgery, Kochi Medical School
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- Yamamoto Tetsuya
- Department of Oral Surgery, Kochi Medical School
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- Ueta Eisaku
- Department of Oral Surgery, Kochi Medical School
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- Osaki Tokio
- Department of Oral Surgery, Kochi Medical School
書誌事項
- タイトル別名
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- Suppression by Azelastine Hydrochloride of NF-/.KAPPA.B Activation Involved in Generation of Cytokines and Nitric Oxide.
- Suppression by Azelastine Hydrochloride
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The influence of the anti-allergy agent azelastine hydrochloride (Azeptin®)on NF-κB activation associated with the. generation of cytokines and nitric oxide (NO)was investigated in various kinds of human and mouse cells. Azeptin dose-dependently suppressed both DNA and protein synthesis in human gingival fibroblasts (HF)and also suppressed blastogenesis of human peripheral blood lymphocytes (PBL). Generation of tumor necrosis factor-alpha, interleukin 1-beta, granulocyte-macrophage colony-stimulating factor and interleukin-6 from 10-5 M Azeptin-treated PBL and human monocytes (HM)was decreased to approximately 1/3 to 2/3 of the control levels. In parallel with the decreased cytokine generation, each cytokine mRNA was less expressed in the presence of 10-5 M Azeptin. In addition, both inducible nitric oxide synthase-mRNA level and NO generation in mouse peritoneal macrophages were suppressed by 10-5 M Azeptin. Being compatible with those results, Azeptin (10-5 M)suppressed activation of NF-κB in PBL, HM and HF. These results appear to indicate that suppression of cytokine and NO generation by Azeptin results at least partially from the inhibition of NF-κB activation.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 73 (2), 145-153, 1997
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204286962048
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- NII論文ID
- 10008677145
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- NII書誌ID
- AA00691188
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- COI
- 1:CAS:528:DyaK2sXhsVWnu7k%3D
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- ISSN
- 13473506
- 00215198
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- NDL書誌ID
- 4153689
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- PubMed
- 9074948
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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
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- 抄録ライセンスフラグ
- 使用不可