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Cardioprotective effect of lycopene against isoproterenol-induced myocardial infarction in rats

机译:番茄红素对异丙肾上腺素致大鼠心肌梗死的心脏保护作用

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摘要

The present study was designed to evaluate the cardioprotective potential of lycopene (LCP) against isoproterenol (ISP)-induced myocardial infarction (MI), by assessing hemodynamic, biochemical and histopathological parameters. Wistar male albino rats were orally administered with LCP (0.5, 1.0 and 1.5 mg/kg) or with vehicle for 30 days, with concurrent subcutaneous injections of ISP (85 mg/kg) on days 28 and 29. ISP significantly (p < 0.05) decreased systolic, diastolic and mean arterial blood pressure (SAP, DAP and MAP, respectively) and heart rate (HR). ISP also decreased contractility (+LVdP/dt), relaxation (-LVdP/dt) and increased left ventricular end-diastolic pressure (LVEDP). In addition to functional impairment, ISP also caused a significant (p < 0.05) decrease in antioxidants, namely, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), glutathione (GSH), cardiac injury marker enzymes, creatine phosphokinase-MB (CK-MB) and lactate dehydrogenase (LDH), as well as induced lipid peroxidation, malonaldialdehyde (MDA) and histopathological alterations in heart. However, pretreatment with LCP significantly (p < 0.05) attenuated ISP-induced cardiac dysfunction as evidenced by improved SAP, DAP, MAP, HR, (±)LVdP/dt and reduced LVEDP. Pretreatment with LCP also significantly (p < 0.05) prevented the depletion of antioxidants (SOD, CAT, GSHPx and GSH), myocyte injury marker enzymes (CK-MB and LDH) and inhibited lipid peroxidation and MDA formation in the heart. Furthermore, reduced necrosis, edema and infiltration of inflammatory cells on histopathological examination also depicted the protective effect of LCP against the deleterious effect of ISP. Based on the results, it is suggested that LCP possesses significant cardioprotective potential and may serve as an adjunct in treatment and prophylaxis of MI.
机译:本研究旨在通过评估血流动力学,生化和组织病理学参数,评估番茄红素(LCP)对异丙肾上腺素(ISP)诱发的心肌梗塞(MI)的心脏保护作用。对Wistar雄性白化病大鼠口服LCP(0.5、1.0和1.5 mg / kg)或载体30天,并在第28和29天同时皮下注射ISP(85 mg / kg)。ISP显着(p <0.05 )降低了收缩压,舒张压和平均动脉压(分别为SAP,DAP和MAP)和心率(HR)。 ISP还降低了收缩力(+ LVdP / dt),放松(-LVdP / dt)和左心室舒张末期压力(LVEDP)升高。除功能障碍外,ISP还引起抗氧化剂的显着降低(p <0.05),即超氧化物歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSHPx),谷胱甘肽(GSH),心脏损伤标记酶,肌酸磷酸激酶MB(CK-MB)和乳酸脱氢酶(LDH),以及诱导的脂质过氧化,丙二醛(MDA)和心脏的组织病理学改变。然而,LCP预处理显着(p <0.05)减轻了ISP引起的心脏功能障碍,SAP,DAP,MAP,HR,(±)LVdP / dt改善和LVEDP降低证明了这一点。用LCP预处理还可以显着(p <0.05)防止抗氧化剂(SOD,CAT,GSHPx和GSH),心肌细胞损伤标记酶(CK-MB和LDH)的消耗,并抑制心脏中脂质过氧化和MDA的形成。此外,在组织病理学检查中,坏死,水肿和炎症细胞浸润的减少也说明了LCP对ISP有害作用的保护作用。根据这些结果,建议LCP具有显着的心脏保护潜力,并且可以作为MI的治疗和预防的辅助手段。

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