NSAIDs diclofenac, indomethacin, and meloxicam highly upregulate expression of ICAM-1 and COX-2 induced by X-irradiation in human endothelial cells

2016 Fiscal Year Final Research Report

• Project/Area Number: 26670547
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Radiation science
• Research Institution: Tohoku University
• Principal Investigator: Hosoi Yoshio 東北大学, 医学系研究科, 教授 (50238747)
• Co-Investigator(Renkei-kenkyūsha): UEHARA Yoshihiko 東北大学, 医学系研究科, 助教 (30223499)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 放射線 / 血管内皮細胞 / 非ステロイド性抗炎症薬 / ICM-1

Outline of Final Research Achievements

Effects of non-steroidal antiinflammatory drugs (NSAIDs) on radiation-induced expression of ICAM-1, VCAM-1, E-selectin, and COX-2 were investigated in human umbilical vein endothelial cells (HUVECs). As NSAIDs, diclofenac, etodolac, indomethacin, ketoprofen, meloxicam, and rofecoxib were used. Irradiation with 10 Gy increased expression of ICAM-1 and COX-2, but it did not affect expression of VCAM-1 or E-selectin. All the NSAIDs upregulated radiation-induced expression of ICAM-1 and COX-2. The extent of upregulation varied depending on the types of NSAIDs. Indomethacin, diclofenac, and meloxicam highly upregulated radiation-induced expression of ICAM-1 and COX-2. The extentof upregulation was not related to the degree of COX-2 selectivity. An NF-kB inhibitor BAY 11-7082 suppressed radiation-induced expression of ICAM-1, but it did not suppress upregulated expression of ICAM-1 or COX-2 by combination treatment with X-irradiation and meloxicam.

Free Research Field

放射線生物学