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dc.contributor.authorSeyed toutounchi, Seyedeh Negisa
dc.date.accessioned2021-05-25T06:25:56Z
dc.date.available2021-05-25T06:25:56Z
dc.date.issued2016en_US
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/64222
dc.description.abstractBackground: rosmarinic acid (RA) is a polyphenolic compound with strong antioxidant activity in biological systems, which makes it a suitable drug candidate in ischemic diseases. Aim: we aimed to investigate the cardioprotective effects of rosmarinic acid in isoproterenol-induced myocardial infarction in rats. Materials and methods: Male wistar rats were assigned to 5 groups of control, isoproterenol, and treatments with 10, 20, 40 mg/Kg of rosmarinic acid. Myocardial infarction was induced by subcutaneous injection of isoproterenol (100 mg/Kg) once daily for 2 days and rosmarinic acid was injected intraperitoneally once daily for 4 days. In fifth day the animals were anesthetized and hemodynamic and electrocardiographic parameters were recorded. After collecting the blood samples, the hearts were removed, washed and weighed immediately to evaluate the cardiac enlargement and were used for further histological studies. Data were analyzed using One-way-ANOVA test and any differences between groups were considered significant at P<0.05. Results: Isoproterenol injection induced cardiac arrhythmias, inflammatory responses, myocardial damage and cardiac hypertrophy. The neutrophil percentage and cardiac hypertrophy were significantly decreased by all doses of rosmarinic acid. All doses of RA also inhibited ST-segment elevation and R-amplitude depression in infarcted hearts. The hemodynamic data analysis showed significant increase in mean arterial pressure and heart rate with different doses of RA compared to isoproterenol group. The left ventricular end diastolic pressure was decreased significantly with RA and the ventricular contractility significantly improved to the normal level with low doses of RA. Also, Histopathological evaluations showed that RA significantly diminished the post MI necrosis and fibrosis in heart and inhibited cardiac hypertrophy, and reduced myocardial MDA level. Conclusion: Results revealed that rosmarinic acid can improve the hemodynamic factors and reduce the myocardial hypertrophy and cell damage after MI, due to its anti-oxidative activity.en_US
dc.language.isoenen_US
dc.publisherTabriz University of Medical Sciences, Faculty of Pharmacyen_US
dc.subjectrosmarinic aciden_US
dc.subjectMyocardial infarctionen_US
dc.subjectIsoproterenolen_US
dc.titleCardioprotective effects of rosmarinic acid in isoproterenol-induced myocardial infarction in ratsen_US
dc.typeThesisen_US
dc.contributor.supervisorGarjani, Alireza
dc.contributor.supervisorFathiazad, Fatemeh
dc.identifier.callno3796en_US
dc.description.disciplinepharmacyen_US
dc.description.degreePharm Den_US


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