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.
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.