本研究以橙皮水萃物 (Water extract of Citrus sinensis；WESP ) 及其生物活性化合物橙皮苷 (Hesperidin；HD)，進行體內氧化壓力下的保肝作用。管灌餵食大鼠 WESP (10、100 mg/kg ) 連續28天後腹腔注射 CCl4 (2 ml/kg bw) ，呈現降低天門冬胺酸胺基轉移酶（AST）和丙胺酸胺基轉移酶（ALT），並改善大鼠肝組織學結構。此外，WESP增加肝還原型麩胱甘肽（GSH）含量，進而導致脂質過氧化指數硫代巴比妥酸反應物質（TBARS）含量降低，並顯著增加超氧化物歧化酶（SOD）和麩胱甘肽過氧化酶（GPx）活性。WESP顯著誘導 CYP2E1 活性，這說明 WESP 可能是誘導 CYP2E1 的受質或活化劑。而WESP (1 mg/kg ) 及 HD (0.1 mg/kg ) 在氧化壓力下無法達到對體內的保護作用。本研究結果顯示橙皮能保護受CCl4誘導的急性肝臟損傷，進而減輕肝臟氧化壓力。這也說明 WESP 可以做為用於治療急性肝臟損傷的保肝劑。 The hepatoprotective effect of water extracts of sweet orange (Citrus sinensis) peel (WESP) and its biological compound, hesperidin (HD), on oxidative stress in vivo, are investigated. Oral administration of WESP to rats at 10 and 100 mg/kg bw for 28 consecutive days before a single dose of CCl4 (2 ml/kg bw) demonstrates a significant protective effect by lowering the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and by improving the histological architecture of the rat liver. In addition, WESP attenuates oxidative stress by increasing the content of hepatic glutathione (GSH), which results in a reduction in the levels of thiobarbituric acid reactive substances (TBARs),the index of lipid peroxidation, and by a dramatic increase in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). WESP induces significant CYP2E1 activity, which suggests that WESP may be a substrate or activator of CYP2E1. WESP at a dose of 1.0 mg/kg bw and HD at 0.1 mg/kg bw does not sustain the protective effect against oxidative stress, in vivo. This study demonstrates that citrus peel protects rat liver from CCl4-induced injury by attenuating hepatic oxidative stress, which suggests that WESP can be used as a therapeutic antihepatotoxic agent for the treatment of hepatic injury.
