本研究為探討紅藜水萃取物 (WECF) 及其活性成分對於四氯化碳 (CCl4) 及酒精引起的肝損傷是否具有保護的作用。管餵受試鼠 WECF (2.5 mg/kg bw) 28天後施打CCl4，結果顯示顯著降低施打CCl4 後增加的天門冬胺酸轉胺酶 (AST) 和丙胺酸轉胺酶 (ALT) 濃度及減輕組織病理切片損害的情況。施打CCl4大鼠並管餵WECF能抑制脂質過氧化，恢復穀胱甘肽 (GSH) 含量，提升超氧化物歧化酶 (SOD) 酵素活性，以及降低淋巴球DNA損傷。施打CCl4 大鼠並管餵1.0 μg/kg bw 蘆丁 (Rutin) 、山奈酚 (Kaempherol) 及甜菜甘 (Betanin)，能恢復GSH含量以及降低淋巴球DNA損傷；而施打CCl4大鼠並管餵Betanin大鼠能提高SOD的活性。連續90天飲用酒精水並管餵受試鼠 1-2.5 mg/kg 的WECF與單獨飲用酒精水的受試鼠比較，結果顯示顯著減輕肝臟組織氧化損害；WECF能抑制飲用酒精水大鼠的脂質過氧化，恢復GSH含量，提升過氧化氫酶 (CAT) 酵素活性，降低細胞色素P450 2E1 (CYP2E1) 活性以及降低淋巴球DNA損傷。飲用酒精水大鼠並管餵 Rutin、Kaempherol 及 Betanin (1.0 μg/kg bw)，能降低淋巴球DNA損傷以及抑制脂質過氧化的發生；而飲用酒精水大鼠並管餵 Rutin 能提高SOD的活性，恢復GSH含量，若管餵Betanin則會增加CYP2E1活性。綜合上述，WECF具有降低氧化壓力的能力，而保護大鼠肝臟來自於CCl4及酒精引起的肝損傷，顯示WECF中所含的活性成分可能負責一定程度WECF的護肝作用。 The protective effect of water extracts of Djulis (Chemopodium formosaneum) (WECF) and its bioactive compounds against carbon tetrachloride-induced and alcohol-induced liver injury in rats was investigated. Oral administration of WECF to rats at 2.5 mg/kg bw for 28 consecutive days before a single dose of CCl4 demonstrated a significantly lowered aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, and attenuated histopathological changes in CCl4-treated rats. WECF inhibited lipid peroxidation, restored glutathione (GSH), enhanced superoxide dismutase (SOD), and reduced lymphocyte DNA damage in CCl4-treated rats. Rutin, kaempherol and betanin at 1.0 μg/kg bw restored GSH levels and reduced lymphocyte DNA damage in CCl4-treated rats. Besides, betanin increased SOD activity in CCl4-treated rats. Oral administration of WECF to rats at 1-2.5 mg/kg bw for 90 consecutive days with the ethanol water intake demonstrated a significantly attenuated histopathological changes in ethanol water-treated rats. WECF inhibited lipid peroxidation, recovery glutathione (GSH), enhanced catalase (CAT), reduced cytochrome P450 2E1 (CYP2E1) and reduced lymphocyte DNA damage in ethanol water-treated rats. Rutin, kaempherol and betanin at 1.0 μg/kg bw reduced lymphocyte DNA damage and inhibited lipid peroxidation in ethanol water-treated rats. In addition, Rutin increased SOD activity and recovery GSH level. Betanin increased CYP2E1 activity in ethanol water-treated rats. Taken together, WECF protects rat liver from CCl4- and ethanol water-treated liver injury due mainly to attenuating oxidative stress. The presence of bioactive compounds in WECF may partly be responsible for the hepatoprotection of WECF.
