The anti-inflammatory effects of anacardic acid on a tnf-α-induced human saphenous vein endothelial cell culture model

Onal B., Ozen D., Demir B., Ak D. , DURSUN E. , Demir C., ...Daha Fazla

Current Pharmaceutical Biotechnology, cilt.21, sa.8, ss.710-719, 2020 (SCI Expanded İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 21 Konu: 8
  • Basım Tarihi: 2020
  • Doi Numarası: 10.2174/1389201020666191105154619
  • Dergi Adı: Current Pharmaceutical Biotechnology
  • Sayfa Sayıları: ss.710-719


© 2020 Bentham Science Publishers.Background and Objective: Coronary bypass operations are commonly performed for the treatment of ischemic heart diseases. Coronary artery bypass surgery with autologous human saphe-nous vein maintains its importance as a commonly used therapy for advanced atherosclerosis. Vascular inflammation-related intimal hyperplasia and atherosclerotic progress have major roles in the patho-genesis of saphenous vein graft disease. Methods: In our study, we investigated the effect of anacardic acid (AA), which is a bioactive phyto-chemical in the shell of Anacardium occidentale, on atherosclerosis considering its inhibitory effect on NF-κB. We observed relative ICAM-1 and NF-κB mRNA levels by qRT-PCR method in a TNF-α-induced inflammation model of saphenous vein endothelial cell culture after 0.1, 0.5, 1 and 5 µM of AA were applied to the cells. In addition, protein levels of ICAM-1 and NF-κB were evaluated by im-munofluorescent staining. The results were compared between different concentrations of AA, and also with the control group. Results: It was found that 5 µM, 1 µM and 0.5 µM of AA had toxic effects, while cytotoxicity decreased when 0.1 µM of AA was applied both alone and with TNF-α. When AA was applied with TNF-α, there was a decrease and suppression in NF-κB expression compared with the TNF-α group. TNF-α-induced ICAM-1 expression was significantly reduced more in the AA-applied group than in the TNF-α group. Conclusion: In accordance with our results, it can be said that AA has a protective role in the patho-genesis of atherosclerosis and hence in saphenous vein graft disease.