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首页> 外文期刊>Biological trace element research >Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities
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Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities

机译:咖啡酸通过抑制血管紧张素转换酶活性和调节脂质谱,葡甘油生成和核苷酸水解酶活性来保护铁诱导的心脏毒性

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摘要

The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO_4. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO_4. Cardiotoxicity induction significantly (p < 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogenphosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (p < 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch.
机译:在铁诱导的心脏毒性中,研究了咖啡酸对血管紧张素转换酶(ACE)和嘌呤能酶活性以及糖异生的保护作用。用0.1 mM FeSO_4在健康雄性SD大鼠的心脏组织中诱导心脏毒性。通过将心脏组织与咖啡酸和0.1 mM FeSO_4共同培养进行治疗。心脏毒性诱导显著(p<0.05)降低了GSH水平、SOD、过氧化氢酶和ENTPDase活性,同时升高了丙二醛(MDA)、一氧化氮、ACE、ATP酶、糖原磷酸化酶、葡萄糖6-磷酸酶、果糖6-双磷酸酶和脂肪酶活性。咖啡酸治疗后,这些水平和活性显著(p<0.05)逆转。咖啡酸还导致心脏胆固醇、甘油三酯、低密度脂蛋白胆固醇水平降低,同时高密度脂蛋白胆固醇水平升高。我们的结果表明,咖啡酸对铁介导的心脏毒性具有保护作用,其抑制氧化失衡和ACE活性的能力,同时调节核苷酸水解和代谢开关。

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