目的 本研究擬探討台灣產獼猴桃屬植物對四氯化碳誘發大鼠急性肝損傷的影響，以期開發台灣固有藥用植物資源。方法 本研究探討台灣產獼猴桃屬植物闊葉獼猴桃(Actinidia latifolia (Gardn. & Champ.) Merr.)、台灣羊桃(A. cbinensis P(下標 LAVCH) var．setosa Li)、紅莖獼猴桃(A. rubricaulis Dunn)與硬齒獼猴桃(A. collosa Lindl.)等四種50%乙醇提取物口服給予大鼠，1小時後腹腔注射四氯化碳，24小時後將大鼠以乙醚麻醉，由頸動脈抽血、離心並取得血清，以測定sGOT、sGPT值與觀察肝損傷病理切片為指標，探討四種不同提取物對四氯化碳致大鼠急性肝炎的保護作用。結果 紅莖獼猴桃(Actinidia rubricaulis Dunn)在各個劑量及硬齒獼猴桃中低劑量(0.1，0.5g/kg)均能抑制四氯化碳誘導大鼠急性肝炎所致大鼠血清sGOT數值(p<0.001)，闊葉獼猴桃及台灣羊桃則無明顯效果。而紅莖獼猴桃在中、高劑量下能增加大鼠肝組織之SOD含量(p<0.01)。又由肝組織病理切片觀察得知，紅莖獼猴桃對四氯化碳誘導大鼠急性肝損傷之肝細胞浸潤及局部壞死具有一定的保護作用。結論 紅莖獼猴桃及硬齒獼猴桃對四氯化碳誘發大鼠急性肝炎具有保護作用，闊葉獼猴桃及台彎羊桃對四氯化碳誘發大鼠急性肝炎不具保護作用。紅莖獼猴桃之肝保護機轉可能與增加肝組織中SOD含量有關。
Purpose. The present study was designed to evaluate the hepatoprotective effect of four Taiwan species of Actinidia on acute liver damage induced by carbon tetrachioride (CCL) in rats. Methods. The extracts of four Actinidia species, Actinidia latifolia (Gardn. & Champ.) Merr. (abrr. AL), A. chinensis P(subscript LANCH) var. setosa Li (ACS), A. rubricaulis Dunn (AR), and A. collosa Lindl. (AC) were orally administered to rats at three doses (0.1, 0.5, 1.0g/kg). Liver damage was induced by CCl4 via an intraperitoneal injection one hour later. Twenty-four hours after CCl4 had been injected, the rats were anaesthetized with ether and blood samples were collected via carotid. The blood was centrifuged at 3000 rpm for 10 minutes and the amounts of serum glutamic-oxalocetic transaminase (sGOT), and serum glutamic-pyruvic transaminase (sGPT) were determined. The hepatoprotective effect of the four extracts in CC14-induced injuries were judged by morphological and biochemical observation. Results. At low doses (0.1, 0.5g/kg), AR and AC inhibited the CCl4-induced liver injury. AR and AC significantly decreased the CCl4-induced increase of sGOT level (p<0.001) and AR (0.1g/kg) decreased the CCl4-induced increase of sGPT level (p<0.05). At high doses (0.5, 1.0g/kg), AR increased SOD activities in the liver (p<0.01), thereby protecting the liver from hepatocytes necrosis. Conclusions. AR and AC seem to inhibit CCl4-induced acute liver injury whereas AL and ACS do not. The mechanism by which AR inhibits liver damage seems to be related to the AR-induced increase in SOD in liver.
