Ajith T A, Hema U, Aswathy M S
Department of Biochemistry, Amala Institute of Medical Sciences, Amala Nagar, Thrissur, Kerala 680 555, India.
Food Chem Toxicol. 2007 Nov;45(11):2267-72. doi: 10.1016/j.fct.2007.06.001. Epub 2007 Jun 9.
A large number of xenobiotics are reported to be potentially hepatotoxic. Free radicals generated from the xenobiotic metabolism can induce lesions of the liver and react with the basic cellular constituents - proteins, lipids, RNA and DNA. Hepatoprotective activity of aqueous ethanol extract of Zingiber officinale was evaluated against single dose of acetaminophen-induced (3g/kg, p.o.) acute hepatotoxicity in rat. Aqueous extract of Z. officinale significantly protected the hepatotoxicity as evident from the activities of serum transaminase and alkaline phosphatase (ALP). Serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT) and ALP activities were significantly (p<0.01) elevated in the acetaminophen alone treated animals. Antioxidant status in liver such as activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase and glutathione-S-transferase (GST), a phase II enzyme, and levels of reduced glutathione (GSH) were declined significantly (p<0.01) in the acetaminophen alone treated animals (control group). Hepatic lipid peroxidation was enhanced significantly (p<0.01) in the control group. Administration of single dose of aqueous extract of Z. officinale (200 and 400mg/kg, p.o.) prior to acetaminophen significantly declines the activities of serum transaminases and ALP. Further the hepatic antioxidant status was enhanced in the Z. officinale plus acetaminophen treated group than the control group. The results of the present study concluded that the hepatoprotective effect of aqueous ethanol extract of Z. officinale against acetaminophen-induced acute toxicity is mediated either by preventing the decline of hepatic antioxidant status or due to its direct radical scavenging capacity.
据报道，大量外源性化学物质具有潜在的肝毒性。外源性化学物质代谢产生的自由基可诱发肝脏损伤，并与基本的细胞成分（蛋白质、脂质、RNA和DNA）发生反应。评价了生姜水乙醇提取物对大鼠单次给予对乙酰氨基酚（3g/kg，口服）诱导的急性肝毒性的保肝活性。生姜水提取物对肝毒性有显著的保护作用，血清转氨酶和碱性磷酸酶（ALP）的活性可证明这一点。在仅用对乙酰氨基酚治疗的动物中，血清谷氨酸丙酮酸转氨酶（SGPT）、血清谷氨酸草酰乙酸转氨酶（SGOT）和ALP活性显著升高（p<0.01）。在仅用对乙酰氨基酚治疗的动物（对照组）中，肝脏中的抗氧化状态，如超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶和谷胱甘肽-S-转移酶（GST，一种II期酶）的活性以及还原型谷胱甘肽（GSH）的水平显著下降（p<0.01）。对照组肝脏脂质过氧化显著增强（p<0.01）。在给予对乙酰氨基酚之前，单次口服生姜水提取物（200和400mg/kg）可显著降低血清转氨酶和ALP的活性。此外，生姜加对乙酰氨基酚治疗组的肝脏抗氧化状态比对照组增强。本研究结果得出结论，生姜水乙醇提取物对乙酰氨基酚诱导的急性毒性的保肝作用是通过防止肝脏抗氧化状态下降或因其直接的自由基清除能力介导的。
