Belkis Atasever Arslan, Fatih Ozen, Tunc Catal, Emine Akalin
{"title":"Resin extract obtained from Cilician fir (Abies Cilicica) inhibits glucose dependent inflammation in vitro.","authors":"Belkis Atasever Arslan, Fatih Ozen, Tunc Catal, Emine Akalin","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The potential anti-inflammatory efficacy of resin extract of Abies cilicica in glucose dependent inflammation and tumor necrosis factor alpha (TNF-a) induced inflammation models was investigated. Its effects on monocyte adhesion, gene expression levels of P-selectin, ICAM-1, VCAM1 and transendothelial migration for the two in vitro models were measured. Also, total flavonoid and total phenolic contents of the extract were determined.</p><p><strong>Objective: </strong>Monocyte adhesion tests showed that the extract increased 100% inflammatory effect of TNF-a induced inflammation. On the other hand, it did not change number of adherent monocytes in glucose dependent inflammation model. Although the extract has trigger effect on monocyte adhesion, it did not change migration of leukocytes across ECV304 cells after administration of TNFa on ECV304 cells. The number of migrated monocytes was similar with only TNFa incubation experiment results. However, it significantly decreased monocyte migration in glucose dependent inflammation model. In our both experimental inflammation model, ICAM-1 expression significantly decreased. Although it is known that triggering effect of TNF-a on ICAM-1 expression, the content of of resin extract of A. cilicica prevented this effect. Phenolic antioxidant capacity of the extract are higher than its flavonoid contents.This study provides the first evidence that the extract inhibits glucose dependent inflammation. It may serve as an anti-inflammatory agent in the treatment of chronic inflammation caused by diabetes.</p>","PeriodicalId":45335,"journal":{"name":"Journal of Experimental Therapeutics and Oncology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Experimental Therapeutics and Oncology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The potential anti-inflammatory efficacy of resin extract of Abies cilicica in glucose dependent inflammation and tumor necrosis factor alpha (TNF-a) induced inflammation models was investigated. Its effects on monocyte adhesion, gene expression levels of P-selectin, ICAM-1, VCAM1 and transendothelial migration for the two in vitro models were measured. Also, total flavonoid and total phenolic contents of the extract were determined.
Objective: Monocyte adhesion tests showed that the extract increased 100% inflammatory effect of TNF-a induced inflammation. On the other hand, it did not change number of adherent monocytes in glucose dependent inflammation model. Although the extract has trigger effect on monocyte adhesion, it did not change migration of leukocytes across ECV304 cells after administration of TNFa on ECV304 cells. The number of migrated monocytes was similar with only TNFa incubation experiment results. However, it significantly decreased monocyte migration in glucose dependent inflammation model. In our both experimental inflammation model, ICAM-1 expression significantly decreased. Although it is known that triggering effect of TNF-a on ICAM-1 expression, the content of of resin extract of A. cilicica prevented this effect. Phenolic antioxidant capacity of the extract are higher than its flavonoid contents.This study provides the first evidence that the extract inhibits glucose dependent inflammation. It may serve as an anti-inflammatory agent in the treatment of chronic inflammation caused by diabetes.