Hwang Yong Pil, Choi Jae Ho, Jeong Hye Gwang
BK 21 Project Team, Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials, Chosun University, 375 Seosuk-dong, Gwangju 501-759, Republic of Korea.
Food Chem Toxicol. 2009 Jan;47(1):75-81. doi: 10.1016/j.fct.2008.10.011. Epub 2008 Oct 17.
The root of Aralia continentalis Kitagawa has been used in traditional Korean medicine to relieve pain and to treat inflammation. The purpose of this study was to investigate the protective effects of the extract of A. continentalis roots (AC) against hepatotoxicity induced by carbon tetrachloride (CCl4) and the mechanism of its hepatoprotective effect. In mice, pretreatment with AC prior to the administration of CCl4 significantly prevented the increased serum enzymatic activity of ALT and AST as well as the formation of hepatic malondialdehyde. Histopathological evaluation of the livers also revealed that AC reduced the incidence of liver lesions induced by CCl4. In addition, pretreatment with AC significantly prevented both the depletion of reduced glutathione (GSH) content and the decrease in glutathione-S-transferase (GST) activity in the liver of CCl4-intoxicated mice. Hepatic GSH levels and GST activity were increased by treatment with AC alone. Heme oxygenase-1 (HO-1) is known to be induced by oxidative stress and to confer protection against oxidative tissue injuries. Interestingly, AC markedly upregulated hepatic HO-1 expression in CCl4-treated mice, which might provide anti-oxidative activity in the liver. These results indicate that AC plays a critical protective role in CCl4-induced acute liver injury by promoting anti-oxidative protein expression.
东北土当归根在传统韩医中用于止痛和治疗炎症。本研究旨在探讨东北土当归根提取物(AC)对四氯化碳(CCl4)诱导的肝毒性的保护作用及其肝保护作用机制。在小鼠中,在给予CCl4之前用AC预处理可显著预防ALT和AST血清酶活性的升高以及肝丙二醛的形成。肝脏的组织病理学评估还显示,AC降低了CCl4诱导的肝脏病变发生率。此外,用AC预处理可显著预防CCl4中毒小鼠肝脏中还原型谷胱甘肽(GSH)含量的消耗和谷胱甘肽-S-转移酶(GST)活性的降低。单独用AC处理可增加肝脏GSH水平和GST活性。血红素加氧酶-1(HO-1)已知可由氧化应激诱导并赋予对氧化性组织损伤的保护作用。有趣的是,AC显著上调了CCl4处理小鼠肝脏中HO-1的表达,这可能在肝脏中提供抗氧化活性。这些结果表明,AC通过促进抗氧化蛋白表达在CCl4诱导的急性肝损伤中起关键保护作用。