Abstract
Background and Objective: Coronary bypass operations are commonly performed for the treatment of ischemic heart diseases. Coronary artery bypass surgery with autologous human saphenous 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 pathogenesis of saphenous vein graft disease.
Methods: In our study, we investigated the effect of anacardic acid (AA), which is a bioactive phytochemical 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 immunofluorescent 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 pathogenesis of atherosclerosis and hence in saphenous vein graft disease.
Keywords: Coronary bypass, anacardic acid, saphenous vein, atherosclerosis, inflammation, NF-κB.
Graphical Abstract
[http://dx.doi.org/10.1056/NEJM197608192950805] [PMID: 778621]
[PMID: 374047]
[http://dx.doi.org/10.1146/annurev.iy.12.040194.001041] [PMID: 8011280]
[PMID: 8497124]
[http://dx.doi.org/10.1152/ajpheart.00252.2015] [PMID: 26945075]
[http://dx.doi.org/10.1111/j.1742-7843.2011.00833.x] [PMID: 22103711]
[http://dx.doi.org/10.3171/2010.12.JNS10588] [PMID: 21275565]
[http://dx.doi.org/10.1182/blood-2007-10-117994] [PMID: 18349320]
[http://dx.doi.org/10.1097/00001573-199411000-00001] [PMID: 7819621]
[http://dx.doi.org/10.1016/S1010-7940(96)80135-7] [PMID: 8664004]
[http://dx.doi.org/10.1590/S0102-76382008000300002] [PMID: 19082314]
[http://dx.doi.org/10.1139/cjpp-2013-0445] [PMID: 24933515]
[http://dx.doi.org/10.1371/journal.pone.0188605] [PMID: 29176823]
[http://dx.doi.org/10.1016/S0022-5347(17)42384-6] [PMID: 3339723]
[http://dx.doi.org/10.1021/acschemneuro.7b00245] [PMID: 28707894]
[http://dx.doi.org/10.1016/j.jchemneu.2016.11.007] [PMID: 27914953]
[http://dx.doi.org/10.1007/s12017-018-8498-6] [PMID: 29948923]
[http://dx.doi.org/10.1016/j.toxlet.2014.05.012] [PMID: 24853302]
[http://dx.doi.org/10.1016/j.bbrc.2012.07.110] [PMID: 22842465]
[http://dx.doi.org/10.1128/MCB.25.18.7966-7975.2005] [PMID: 16135789]
[http://dx.doi.org/10.1016/S0003-4975(03)00433-8] [PMID: 12902083]
[http://dx.doi.org/10.1016/S0003-4975(98)00274-4] [PMID: 9647082]
[http://dx.doi.org/10.1016/j.prostaglandins.2013.06.001] [PMID: 23770055]
[http://dx.doi.org/10.1161/01.ATV.0000160340.72641.87] [PMID: 15731497]
[http://dx.doi.org/10.1016/S0735-1097(01)01377-8] [PMID: 11499717]
[http://dx.doi.org/10.1097/SLA.0b013e318288c38d] [PMID: 23574989]
[http://dx.doi.org/10.1016/S0828-282X(09)70486-6] [PMID: 19214303]
[http://dx.doi.org/10.1146/annurev.ph.57.030195.004143] [PMID: 7778885]
[http://dx.doi.org/10.1016/j.jnutbio.2003.11.008] [PMID: 15068815]
[http://dx.doi.org/10.1016/j.ejphar.2015.03.014] [PMID: 25797284]