2008年行政院衛生署所統計之國人十大死因中慢性肝炎及肝硬化排名第七位,顯示肝病之防治及治療為目前台灣急需改善之健康議題。本實驗之主要目的是以四氯化碳 (carbon tetrachloride, CCl4)誘導急性及慢性肝損傷動物實驗模式評估人參雞精 (ginseng-based chicken essence, GCE)之護肝保健功效。急性實驗將Wistar大鼠分成六組,分別為控制組、四氯化碳組、Silymarin 正控制組 (0.5 g/kg bw/day)、低、中及高劑量人參雞精樣品 (0.62、3.12和6.23 g/kg bw/day)組。各組經過連續5天管餵0.5%羧甲基纖維素 (carboxymethyl cellulose, CMC)、Silymarin (0.5 g/kg bw/day)或低、中及高劑量人參雞精樣品 (0.62、3.12和6.23 g/kg bw/day)後,各組於第六天腹腔注射四氯化碳 (40% CCl4 in olive oil,1 ml/kg bw)經18小時後犧牲,採集血液並剖腹取肝臟樣本進行分析。實驗結果顯示,在血清中丙胺酸轉胺酶 (alanine aminotransferase, ALT)和天門冬胺酸轉胺酶 (aspartate aminotransferase, AST)值方面,三種劑量人參雞精樣品組皆低於四氯化碳組,而以高劑量人參雞精樣品 (6.23 g/kg bw/day)組達顯著降低的情形 (p < 0.05)。在抗氧化及解毒代謝酵素及抗氧化物質方面,四氯化碳會顯著降低肝臟中抗氧化物質麩胱甘肽 (glutathione, GSH)含量 (p < 0.05),且降低肝臟中抗氧化及解毒代謝酵素如麩胱甘肽過氧化酶 (glutathione peroxidase, GPx)、麩胱甘肽還原酶 (glutathione reductase, GRd)、麩胱甘肽硫轉移酶 (glutathione S-transferase, GST)、過氧化氫酶 (catalase, CAT)、及超氧化物歧化酶 (superoxide dismutase, SOD)等酵素活性,而人參雞精樣品則能顯著改善上述情形 (p < 0.05)。急性實驗以中劑量人參雞精樣品 (3.12 g/kg bw/day)組對改善四氯化碳所誘導之肝損傷效果最具顯著。而在慢性實驗中,四氯化碳組改以管餵 (20% CCl4 in olive oil,1.5 ml/kg bw)每週管餵兩次,連續進行八週;每日經口給予0.5% CMC、Silymarin或低、中及高劑量人參雞精樣品 (0.62、3.12和6.23 g/kg bw/day)八週後,進行犧牲並採集血液及肝臟樣品作為分析之用。慢性實驗結果顯示,四氯化碳組會較正常大鼠顯著增加肝臟之相對重量 (p < 0.05),而給予人參雞精樣品可顯著改善四氯化碳組肝臟之相對重量增加現象 (p < 0.05);給予低、中及高劑量人參雞精樣品 (0.62、3.12和6.23 g/kg bw/day)較四氯化碳組顯著降低ALT、AST值 (p < 0.05);此外,給予低、中及高劑量人參雞精 (0.62、3.12和6.23 g/kg bw/day)的組別較四氯化碳組可顯著增加大鼠肝臟中還原態GSH含量,及肝臟GPx、GRd、GST、CAT及SOD酵素活性情形 (p < 0.05);此外人參雞精樣品亦可改善四氯化碳所造成肝臟中脂質過氧化物硫代巴比妥酸反應物質 (thiobarbituric acid reactive substances, TBARS)及羥脯胺酸 (hydroxyproline)等含量增加的情形 (p < 0.05)。低劑量人參雞精樣品 (0.62 g/kg bw/day)組即具有顯著改善四氯化碳所誘發之肝損傷情形。因此,綜合以上急性及慢性實驗結果,在四氯化碳所誘導肝損傷模式下,本實驗之人參雞精樣品的確具有護肝功效之潛力。
According to the statistics data of Department of Health Executive Yuan of Taiwan, chronic liver disease and cirrhosis is the seventh leading cause of death in Taiwan in 2008. Preventing and treating liver disease is a public health problem in Taiwan. The aim of this study was to evaluate the hepatoprotective effect of ginseng-based chicken essence (GCE) on carbon tetrachloride (CCl4)-induced acute and chronic liver injuries in rats. In acute experiment, male Wistar rats were randomly divided into six groups: control, CCl4, CCl4 + 0.5 g Silymarin/kg bw/day, CCl4 + 0.62 g GCE/kg bw/day, CCl4 + 3.12 g GCE/kg bw/day, and CCl4 + 6.23 g GCE/kg bw/day. Rats were orally administrated 0.5% carboxymethyl cellulose (CMC), Silymarin, or GCE for consecutive 5 days. After CCl4 (40% in olive oil, 1 ml/kg bw) was intraperitoneally injection on 6th day, rats were sacrificed after 18 hours, and the blood and liver sample were taken for analysis. Compared to CCl4 group, GCE at 6.23 g/kg bw/day showed significant decrease in ALT and AST levels (p < 0.05). The results of hepatic reduced GSH content, antioxidation and detoxification enzyme activities indaicated that CCl4 could significantly lower hepatic GSH, and decrease the activities of glutathione peroxidase (GPx), glutathione reductase (GRd), glutathione S-transferase (GST), catalase (CAT), and superoxide dismutase (SOD) compared to control group (p < 0.05), however, GCE significantly recovered them (p < 0.05). 6.23 g GCE/kg bw/day exhibited significantly protective effects on CCl4-induced acute liver injury in rats. In chronic experiment, liver injury was induced by oral administration with CCl4 (20% in olive oil, 1.5 ml/kg bw), twice a week for 8 weeks. After oral administration of 0.5% CMC, Silymarin or GCE for 8 weeks, rats were sacrificed, and their blood and liver samples were collected for further analysis. The results showed that CCl4 administration could significantly increased liver relative weights compared with the normal control group (p < 0.05), and rats administrated with GCE showed significantly decreased liver relative weights compared with CCl4 group (p < 0.05). Compared to CCl4 groups, oral administration GCE at 0.62 g, 3.12 g, and 6.23 g/kg bw significantly recovered AST and ALT level (p < 0.05), and significantly increased hepatic GSH content, and enzyme activities of GPx, GRd, GST, CAT, and SOD (p < 0.05). Furthermore, GCE treatment could significantly lower the accumulation of hepatic thiobarbituric acid reactive substances (TBARS) and hydroxyproline caused by CCl4 treatment (p < 0.05). The chronic experiment results indicated that 0.62 g GCE/kg bw/day could significantly recover the liver injury caused by CCl4. Based on the results of acute and chronic experiments, GCE samples probably could exert a potential hepatoprotective effects against CCl4-induced liver injury models.