Ferulic Acid Attenuates Adhesion Molecule Expression in Gamma-Radiated Human Umbilical Vascular Endothelial Cells
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- Ma Zeng-Chun
- Beijing Institute of Radiation Medicine
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- Hong Qian
- Beijing Institute of Radiation Medicine
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- Wang Yu-Guang
- Beijing Institute of Radiation Medicine
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- Tan Hong-Ling
- Beijing Institute of Radiation Medicine
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- Xiao Cheng-Rong
- Beijing Institute of Radiation Medicine
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- Liang Qian-De
- Beijing Institute of Radiation Medicine
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- Cai Shao-Hua
- Geriatric-Respiratory Department, PLA General Hospital
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- Gao Yue
- Beijing Institute of Radiation Medicine
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Radiation induces an important inflammatory response in the irradiated organs, characterized by leukocyte infiltration and vascular changes. Since adhesion molecules play an important role in facilitating the immune response at the inflammation sites, interfering with the expression of these molecules may be an important therapeutic target of radiation induced inflammation. Many adhesion molecules such as intercellular cell adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) have been identified in radiation. Ferulic acid (FA), an effective radioprotector during radiotherapy, is widely used in endothelium protection. The present study examined the effect of FA on the induction of adhesion molecules by gamma-radiation and the mechanisms of its effect in gamma-irradiated human umbilical vein endothelial cells (HUVECs). HUVECs were pretreated for 18 h with FA and then exposed to 10 Gy radiation. The result of cell adhesion assay showed FA inhibited radiation-induced U937 adhesion to HUVECs. FA prevented induction of ICAM-1 and VCAM-1 expression in a concentration-dependent manner after stimulation with radiation at the level of mRNA and protein. Inhibitors of the extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways were used to determine which pathway was involved in FA action; the result showed that the inhibitory effect of FA on adhesion molecule expression was mediated by the blockade of JNK. FA appears to be a potential therapeutic agent for treating various inflammatory disorders including radiation induced inflammation.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 33 (5), 752-758, 2010
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
- 1390001204625723904
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- NII論文ID
- 130000248032
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 10662038
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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
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