College of Veterinary Medicine, Chungnam National University, Daejeon 305-764, Korea.
J Ginseng Res. 2011 Jun;35(2):243-9. doi: 10.5142/jgr.2011.35.2.243.
Korean red ginseng (KRG), the steamed root of Panax ginseng Meyer, has a variety of biological properties, including anti-inflammatory, antioxidant and anticancer effects. Aflatoxin B1 (AFB1) produced by the Aspergillus spp. causes acute hepatotoxicity by lipid peroxidation and oxidative DNA damage, and induces liver carcinoma in humans and laboratory animals. This study was performed to examine the protective effects of KRG against hepatotoxicity induced by AFB1 using liver-specific serum marker analysis, histopathology, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. In addition, to elucidate the possible mechanism of hepatoprotective effects, superoxide dismutase, catalase, glutathione peroxidase, and malondialdehyde were analyzed. Rats were treated with 250 mg/kg of KRG (KRG group) or saline (AFB1 group) for 4 weeks and then received 150 μg/kg of AFB1 intraperitoneally for 3 days. Rats were sacrificed at 12 h, 24 h, 48 h, 72 h, or 1 wk after AFB1 treatment. In the KRG pre-treatment group, serum alanine aminotransferase, aspartate aminotransferase, and malondialdehyde levels were low, but superoxide dismutase, catalase, and glutathione peroxidase activities were high as compared to the AFB1 alone group. Histopathologically, AFB1 treatment induced necrosis and apoptosis in hepatocytes, and led to inflammatory cells infiltration in the liver. KRG pre-treatment ameliorated these changes. These results indicate that KRG may have protective effects against hepatotoxicity induced by AFB1 that involve the antioxidant properties of KRG.
韩国红参（KRG）是 Panax ginseng Meyer 的蒸根，具有多种生物特性，包括抗炎、抗氧化和抗癌作用。黄曲霉毒素 B1（AFB1）由曲霉属产生，通过脂质过氧化和氧化 DNA 损伤引起急性肝毒性，并在人类和实验动物中诱导肝癌。本研究旨在通过肝特异性血清标志物分析、组织病理学和末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记来研究 KRG 对 AFB1 诱导的肝毒性的保护作用。此外，为了阐明其可能的保肝作用机制，还分析了超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和丙二醛。大鼠用 250 mg/kg 的 KRG（KRG 组）或生理盐水（AFB1 组）处理 4 周，然后腹膜内注射 150 μg/kg 的 AFB1 3 天。在 AFB1 处理后 12 h、24 h、48 h、72 h 或 1 周处死大鼠。在 KRG 预处理组中，血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶和丙二醛水平较低，但超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性较高。组织病理学检查显示，AFB1 处理诱导肝细胞坏死和凋亡，并导致肝脏中炎症细胞浸润。KRG 预处理可改善这些变化。这些结果表明，KRG 可能对 AFB1 诱导的肝毒性具有保护作用，这与其抗氧化特性有关。
