Department of Pharmacology and Toxicology, Cairo University, Cairo, Egypt.
Arch Iran Med. 2012 Nov;15(11):674-80.
Paracetamol overdose causes severe hepatotoxicity that leads to liver failure in both humans and experimental animals. The present study investigates the protective effect of honey against paracetamol-induced hepatotoxicity in Wistar albino rats. We have used silymarin as a standard reference hepatoprotective drug.
Hepatoprotective activity was assessed by measuring biochemical parameters such as the liver function enzymes, serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). Equally, comparative effects of honey on oxidative stress biomarkers such as malondialdyhyde (MDA), reduced glutathione (GSH) and glutathione peroxidase (GPx) were also evaluated in the rat liver homogenates. We estimated the effect of honey on serum levels and hepatic content of interleukin-1beta (IL-1β) because the initial event in paracetamol-induced hepatotoxicity has been shown to be a toxic-metabolic injury that leads to hepatocyte death, activation of the innate immune response and upregulation of inflammatory cytokines.
Paracetamol caused marked liver damage as noted by significant increased activities of serum AST and ALT as well as the level of Il-1β. Paracetamol also resulted in a significant decrease in liver GSH content and GPx activity which paralleled an increase in Il-1β and MDA levels. Pretreatment with honey and silymarin prior to the administration of paracetamol significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of paracetamol-induced liver lesions.
Honey can be used as an effective hepatoprotective agent against paracetamol-induced liver damage.
对乙酰氨基酚过量会导致严重的肝毒性，在人类和实验动物中都会导致肝衰竭。本研究旨在探讨蜂蜜对 Wistar 白化大鼠乙酰氨基酚诱导肝毒性的保护作用。我们使用水飞蓟素作为标准参考肝保护药物。
通过测量肝功能酶等生化参数，如血清丙氨酸氨基转移酶（ALT）和血清天冬氨酸氨基转移酶（AST），评估肝保护活性。同样，还评估了蜂蜜对丙二醛（MDA）、还原型谷胱甘肽（GSH）和谷胱甘肽过氧化物酶（GPx）等氧化应激生物标志物的影响。我们估计了蜂蜜对血清水平和肝内白细胞介素-1β（IL-1β）的影响，因为在乙酰氨基酚诱导的肝毒性中，最初的事件是一种毒性代谢损伤，导致肝细胞死亡、固有免疫反应的激活和炎症细胞因子的上调。
乙酰氨基酚导致明显的肝损伤，表现为血清 AST 和 ALT 活性以及 IL-1β水平显著升高。乙酰氨基酚还导致肝 GSH 含量和 GPx 活性显著降低，这与 IL-1β和 MDA 水平的升高相平行。在给予乙酰氨基酚之前用蜂蜜和水飞蓟素预处理可显著防止血清肝酶标志物水平的升高，并降低氧化应激和炎症细胞因子。肝组织病理学评估还表明，蜂蜜可减少乙酰氨基酚引起的肝损伤的发生率。
蜂蜜可作为乙酰氨基酚诱导肝损伤的有效肝保护剂。
