{"title":"The Cardioprotective Effects of 4-O-(2″-O-acetyl-6″-O- P-coumaroyl-β-D-glucopyranosyl)-P-coumaric Acid (4-ACGC) on Chronic Heart Failure","authors":"Yong Yang, K. Yu, Yan-min Zhang","doi":"10.22037/IJPR.2018.2188","DOIUrl":null,"url":null,"abstract":"The 4-ACGC isolated from BP was prepared to investigate the cardioprotective effects on attenuating chronic heart failure in-vivo and in-vitro. A chronic heart failure (CHF) rat model was established to investigate the cardioprotective effects of 4-ACGC. From this, several cardiac function indexes were recorded. The inflammatory markers including tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), and Interleukin-1β (IL-1β) were evaluated by enzyme-linked immunosorbent assay (ELISA). Subsequently, serum levels of myocardial enzymes lactate dehydrogenase (LDH) and creatine kinase (CK) were also assessed by ELISA kits. Ultimately, the cardioprotective and anti-inflammatory effects of 4-ACGC were further verified on CMECs. The results showed that the treatment of 4-ACGC significantly reduced cardiac hypertrophy and reversed the Ejection Fraction (EF), Heart Rate (HR), Fractional Shortening (FS), and Cardiac Output (CO) changes in CHF rats. The treatment of 4-ACGC could effectively inhibit the inflammatory cytokines induced by CHF. It’s also showed that a reverse effect of 4-ACGC on serum increased levels of LDH and CK in CHF rats. The increased levels of IL-1β and IL-6 stimulated by TNF-α on CMECs were also decreased after treating with 4-ACGC. The present study provided experimental evidence that 4-ACGC possessed obvious cardioprotective effects on attenuating CHF. 4-ACGC could suppress the expression of inflammatory mediators and myocardial enzymes, which might be one of the mechanisms.","PeriodicalId":416671,"journal":{"name":"Iranian Journal of Pharmaceutical Research : IJPR","volume":"38 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iranian Journal of Pharmaceutical Research : IJPR","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22037/IJPR.2018.2188","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
Abstract
The 4-ACGC isolated from BP was prepared to investigate the cardioprotective effects on attenuating chronic heart failure in-vivo and in-vitro. A chronic heart failure (CHF) rat model was established to investigate the cardioprotective effects of 4-ACGC. From this, several cardiac function indexes were recorded. The inflammatory markers including tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), and Interleukin-1β (IL-1β) were evaluated by enzyme-linked immunosorbent assay (ELISA). Subsequently, serum levels of myocardial enzymes lactate dehydrogenase (LDH) and creatine kinase (CK) were also assessed by ELISA kits. Ultimately, the cardioprotective and anti-inflammatory effects of 4-ACGC were further verified on CMECs. The results showed that the treatment of 4-ACGC significantly reduced cardiac hypertrophy and reversed the Ejection Fraction (EF), Heart Rate (HR), Fractional Shortening (FS), and Cardiac Output (CO) changes in CHF rats. The treatment of 4-ACGC could effectively inhibit the inflammatory cytokines induced by CHF. It’s also showed that a reverse effect of 4-ACGC on serum increased levels of LDH and CK in CHF rats. The increased levels of IL-1β and IL-6 stimulated by TNF-α on CMECs were also decreased after treating with 4-ACGC. The present study provided experimental evidence that 4-ACGC possessed obvious cardioprotective effects on attenuating CHF. 4-ACGC could suppress the expression of inflammatory mediators and myocardial enzymes, which might be one of the mechanisms.