Área Académica de Farmacia, Universidad Autónoma del Estado de Hidalgo, Mariano Abasolo 600, Colonia Centro, Pachuca, Hidalgo CP 42000, Mexico.
Departamento de Farmacología, Farmacognosia y Botánica, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza Ramón y Cajal S/N, 28040 Madrid, Espana.
Molecules. 2019 Jul 11;24(14):2533. doi: 10.3390/molecules24142533.
The aim of this study was to evaluate the antioxidant and hepatoprotective activity of (EC). The present work reports the first pharmacological, toxicological, and antioxidant studies of EC extract on liver injury. Liver necrosis was induced by thioacetamide (TAA). Five groups were established: Extract (EC), thioacetamide (TAA), extract with thioacetamide (EC + TAA), vitamin E with thioacetamide (VE + TAA) and the positive control and vehicle (CT). For EC and EC + TAA, Wistar rats (n = 8) were intragastrically pre-administered for 4 days with EC (300 mg/kg.day) and on the last day, EC + TAA received a single dose of TAA (400 mg/kg). At 24 h after damage induction, animals were sacrificed. In vitro activity and gene expression of superoxide dismutase (SOD), catalase (), and Nrf2 nuclear factor were measured. The results show that EC has medium antioxidant properties, with an IC of 0.63 mg/mL and a ferric-reducing power of 279.8 µM/mg. Additionally, EC reduced hepatic damage markers at 24 h after TAA intoxication; also, it increased and gene expression against TAA by controlling antioxidant defense levels. Our findings demonstrated the hepatoprotective effect of EC by reducing hepatic damage markers and controlling antioxidant defense levels. Further studies are necessary to identify the mechanism of this protection.
本研究旨在评估 (EC)的抗氧化和保肝活性。本工作首次报道了 EC 提取物对肝损伤的药理、毒理和抗氧化研究。肝坏死由硫代乙酰胺(TAA)诱导。建立了 5 组:提取物(EC)、硫代乙酰胺(TAA)、硫代乙酰胺加提取物(EC+TAA)、硫代乙酰胺加维生素 E(VE+TAA)和阳性对照及载体(CT)。对于 EC 和 EC+TAA,Wistar 大鼠(n=8)连续 4 天经胃内给予 EC(300mg/kg·天),最后一天 EC+TAA 给予单次 TAA(400mg/kg)。损伤诱导后 24 小时处死动物。测量超氧化物歧化酶(SOD)、过氧化氢酶()和核因子 Nrf2 的体外活性和基因表达。结果表明,EC 具有中等抗氧化性能,IC 为 0.63mg/mL,铁还原能力为 279.8µM/mg。此外,EC 可降低 TAA 中毒 24 小时后肝损伤标志物;还通过控制抗氧化防御水平增加 和 基因表达。我们的研究结果表明,EC 通过降低肝损伤标志物和控制抗氧化防御水平发挥保肝作用。需要进一步研究以确定这种保护的机制。