褪黑素作为抗高脂饮食心肌损伤的潜在治疗分子

G. Bose, A. Ghosh, A. Chattopadhyay, P. Pal, D. Bandyopadhyay
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引用次数: 2

摘要

自上世纪下半叶以来,高脂肪饮食(HFD)已被认为是心血管疾病的独立危险因素。HFD引起心血管疾病的各种发病机制和进展。HFD诱导的氧化应激和促炎反应可能是心肌损伤的主要危险因素。本文综述了不同膳食脂肪在心血管疾病中的作用,以及褪黑素作为一种有效的抗氧化剂和抗炎症分子对HFD诱导的病理的保护作用。重点将放在分子机制。褪黑素对HFD诱导心肌损伤的保护作用是通过多种途径介导的。其中包括褪黑素抑制氧化应激,保持正常的脂肪和葡萄糖代谢,减少促炎反应。褪黑素下调促炎基因TLR4、NF-κB和NLRP3-Caspase1的表达,上调抗炎基因Sirt3、CTRP3和RISK的表达。所有这些都使褪黑素成为对抗由HFD引起的心血管疾病的强大保护器。这一综述表明,褪黑激素可以作为一种治疗这种特殊情况的药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Melatonin as a potential therapeutic molecule against myocardial damage caused by high fat diet (HFD)
     High fat diet (HFD) has been implicated as an independent risk factor for cardiovascular diseases since the second half of the last century. The HFD causes various pathogeneses and progressions of cardiovascular diseases. The oxidative stress and pro-inflammatory reactions induced by the HFD are probably the major risk factors of myocardial damage. In this review we highlight the roles of different dietary fats on cardiovascular diseases and the protective effects of melatonin as a potent antioxidant and anti-inflammation molecule on the pathology induced by HFD. The focus will be given to the molecular mechanisms. The protective effects of melatonin on HFD induced myocardial damage are mediated by multiple pathways. These include that melatonin suppresses the oxidative stress, preserves the normal fat and glucose metabolisms and reduces the pro-inflammatory reactions. Melatonin downregulates the expressions of pro-inflammatory genes of TLR4, NF-κB and NLRP3-Caspase1 but upregulates the expressions of anti-inflammatory genes of Sirt3, CTRP3 and RISK. All of these render melatonin as a powerful protector against cardiovascular diseases caused by the HFD. This review suggests that melatonin can be used as a therapeutic agent in this specific condition.  
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