Ahlam M. Alhusaini, Hanan K. Alghibiwi, Wedad S. Sarawi, Juman S. Alsaab, Samiyah M. Alshehri, Qamraa H. Alqahtani, Aliah R. Alshanwani, Ebtesam A. Aljassas, Ebtesam N. Alsultan, Iman H. Hasan
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引用次数: 0
摘要
异丙肾上腺素(ISO)是一种化学合成的儿茶酚胺,属于β肾上腺素受体激动剂,用于治疗心动过缓。β肾上腺素能激动剂是心肌新陈代谢和收缩力的重要调节剂;然而,过量接触 ISO 会引发氧化应激和炎症。本研究旨在探讨 ISO 诱导心脏重塑的分子机制、白藜芦醇(RSVR)及其脂质体制剂(L-RSVR)对这种心脏变化的保护作用。将 Wistar 白化大鼠平均分为 4 组。对照组、ISO 组(每周两次,每次 50 毫克/千克,静脉注射)、RSVR 和 L-RSVR 处理组(RSVR 或 L-RSVR(20 毫克/千克/天,口服)与 ISO 同时服用,为期 2 周)。与对照组相比,ISO 导致心脏组织中 BAX 和 MEF2 mRNA、S100A1 和细胞色素 C 蛋白的表达水平以及 DNA 断裂水平明显升高。使用 RSVR 或 L-RSVR 治疗 14 天后,ISO 诱导的损伤明显改善,这体现在所有测量参数的改善上。本研究表明,L-RSVR 对 ISO 诱导的大鼠心脏损伤具有更好的心脏保护作用,这很可能是通过调节心脏 S100A1 蛋白的表达以及抑制炎症和细胞凋亡实现的。
Resveratrol-Based Liposomes Improve Cardiac Remodeling Induced by Isoproterenol Partially by Modulating MEF2, Cytochrome C and S100A1 Expression
Isoproterenol (ISO), a chemically synthesized catecholamine, belongs to β-adrenoceptor agonist used to treat bradycardia. The β-adrenergic agonist is an essential regulator of myocardial metabolism and contractility; however, excessive exposure to ISO can initiate oxidative stress and inflammation. This study aims to investigate the molecular mechanisms underlying ISO-induced cardiac remodeling, the protective efficacy of resveratrol (RSVR), and its liposomal formulation (L-RSVR) against such cardiac change. Wistar albino rats were evenly divided into 4 groups. Control group, ISO group received ISO (50 mg/kg, s.c.) twice a week for 2 weeks, and RSVR- and L-RSVR-treated groups in which rats received either RSVR or L-RSVR (20 mg/kg/day, p.o.) along with ISO for 2 weeks. ISO caused a significant elevation of the expression levels of BAX and MEF2 mRNA, S100A1 and cytochrome C proteins, as well as DNA fragmentation in cardiac tissue compared to the control group. Treatment with either RSVR or L-RSVR for 14 days significantly ameliorated the damage induced by ISO, as evidenced by the improvement of all measured parameters. The present study shows that L-RSVR provides better cardio-protection against ISO-induced cardiac injury in rats, most likely through modulation of cardiac S100A1 protein expression and inhibition of inflammation and apoptosis.