Cardiovascular Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, India.
Hum Exp Toxicol. 2013 May;32(5):492-503. doi: 10.1177/0960327112454890. Epub 2012 Oct 11.
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.
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) 诱导的心肌梗死 (MI) 的心脏保护作用。雄性 Wistar 白化大鼠连续 30 天口服 LCP(0.5、1.0 和 1.5 mg/kg)或载体,同时在第 28 和 29 天皮下注射 ISP(85mg/kg)。ISP 显著降低收缩压、舒张压和平均动脉压(SAP、DAP 和 MAP)和心率(HR)。ISP 还降低收缩力(+LVdP/dt)、舒张功能(-LVdP/dt)并增加左心室舒张末期压(LVEDP)。除了功能障碍外,ISP 还显著降低抗氧化剂,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)、心脏损伤标志物酶肌酸磷酸激酶-MB(CK-MB)和乳酸脱氢酶(LDH),并诱导脂质过氧化,丙二醛(MDA)和心脏组织病理学改变。然而,LCP 预处理显著减轻 ISP 诱导的心脏功能障碍,表现为 SAP、DAP、MAP、HR、(±)LVdP/dt 升高,LVEDP 降低。LCP 预处理还显著防止抗氧化剂(SOD、CAT、GSHPx 和 GSH)、肌细胞损伤标志物酶(CK-MB 和 LDH)耗竭,并抑制心脏脂质过氧化和 MDA 形成。此外,组织病理学检查显示,坏死、水肿和炎症细胞浸润减少,表明 LCP 对 ISP 有害作用具有保护作用。基于这些结果,建议 LCP 具有显著的心脏保护作用,可作为 MI 治疗和预防的辅助手段。