Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats

Abstract

ÖZETAmaç: Kafeik asit fenetil ester (CAPE) güçlü antiinflamatuvar, anti-tümör ve antioksidan özelliklere sahip doğal bir üründür ve iskemireperfüzyonun indüklediği inflamasyonu ve lipid peroksidasyonu azaltır. Bu çalışmanın amacı isoproterenol (ISO) indüklü miyokardiyal infarktüs üzerine CAPE tedavisinin etkilerini incelemektir. Yöntemler: Bu çalışmada rasgele deneysel kontrollü araştırma dizaynı seçildi. Sıçanlar dört gruba ayrıldı: Kontrol, CAPE, ISO, ISO+CAPE. CAPE (10 μmol kg/gün i.p.) ve ISO (150 mg /kg s.c.) tek başlarına ratlara 7 gün süreyle verildi. ISO+CAPE grubunda ise ratlara ISO (150 mg /kg s.c.) uygulamasından 3 gün önce CAPE (10 μmol kg/gün i.p.) verilmeye başlandı. Yedi günlük deney periyodunun sonunda ratlar öldürüldü ve biyokimyasal analizler için kan ve doku örnekleri alındı. Verilerin istatistiksel analizi tek-yönlü ANOVA ve post-hoc LSD testi ile yapıldı. Bulgular: Tek başına ISO uygulanması sonucu myeloperoksidaz (MPO) aktivitesi, lipid peroksidasyonu, süperoksit dismutaz (SOD) ve katalaz (CAT) aktiviteleri arttı. Tek başına CAPE uygulaması ise enzim değerlerini kontrole göre değiştirmedi. CAPE tedavisi verilen grupta ise MPO aktivitesi ve malondialdehit seviyesi düşerken, CAT ve SOD aktivitesi değişmedi. Sonuç: Mevcut bulgular CAPE tedavisinin nötrofil MPO aktivitesini inhibe ederek MPO ve lipid peroksidasyon aracılı miyokardiyal hasarı önle-diğine işaret etmektedir. (Anadolu Kardiyol Derg 2010; 10: 298-302) Anahtar kelimeler: Kafeik asit fenetil ester, isoproterenol, lipid peroksidasyonu, miyokardiyal infarktüs, oksidatif stres, miyeloperoksidaz ABSTRACT Objective: Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction. Methods: A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 μmol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data. Results: The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes. Conclusion: In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil's MPO activity. (Anadolu Kardiyol Derg 2010; 10: 298-302)

The effect of caffeic acid phenethyl ester on isoproterenol-induced myocardial injury in hypertensive rats

“…In the previous studies reported that L-NNA decreases the activities of antioxidant enzymes and enhances lipid peroxidation (29). In accordance with previous studies, it was observed that 150 mg/kg dose of ISO induced a myocardial damage and significantly altered biochemical parameters and antioxidant enzyme activities in the present study (13). In the present study ISO administration caused myocardial damage which was reflected by a significant increase in serum AST and LDH levels.…”

“…Myeloperoxidase (MPO) is a neutrophil and monocyte enzyme that amplifies the reactivity of hydrogen peroxide (33). We did not measure MPO activity, but we previously showed that CAPE decreases the rised MPO activity in heart (13). MPO and its oxidation products can play a key role for the enzyme in promoting of lipid peroxidation and other oxidative modifications in acute myocardial infarction (34).…”

“…CAPE can completely block the production of reactive oxygen species (ROS) in human neutrophils and in the xanthine/xanthine oxidase (XO) system at a concentration of 10 μmol (12). In the previous studies it has been shown that CAPE preserves heart tissue from isoproterenol-induced cardiac damage and restores the impaired antioxidant enzyme activity in the rat kidney and heart (13)(14)(15)(16)(17). Furthermore, it was reported that CAPE (10 μmol/kg) application significantly reversed the increased MDA, decreased NO levels and the increased diameters of myocardial myofibrils in cadmium-induced hypertensive rats (11).…”

Caffeic Acid Phenethyl Ester Suppresses the Production of Adipocytokines, Leptin, Tumor Necrosis Factor -Alpha and Resistin, during Differentiation to Adipocytes in 3T3-L1 Cells

“…28) From this finding, CAPE may attenuate the development of obesity in rodents. Furthermore, the protective effect of CAPE on the development of the cardiovascular system 29,30) and myocardial injury 31) in rodents was documented. This arterial dysfunction is regulated by the expression of adipokines such as, leptin, resistin and TNF-alpha.…”

Recruitment and in situ Renewal Regulate Rapid Accumulation of CD11c+ Cells in the Lung following Intranasal Superantigen Challenge

“…SEA was chosen over SEB since SEA has the ability to bind both MHC IIα and MHC IIβ chains resulting in the upregulation of costimulatory molecules on the APC along with the production of proinflammatory cytokines. This results in more robust T cell stimulation compared to SEB, which better mimics the human situation [24, 25]. …”