枸杞地黃熱水萃取物對於四氯化碳誘發老鼠肝傷害之影響
本研究探討以熱水粗萃取枸杞與地黃中多醣之成分，餵予雄性 Sprague-Dawley 老鼠，
並以四氯化碳 (CCl4) 誘發肝傷害，探討對肝臟病理切片、血漿中肝功能指標、脂質代 謝與抗氧化能力、發炎反應及纖維化的影響。將老鼠隨機分成四組 ( 每組 10 隻 ) ：正 常飲食＋腹腔注射橄欖油、正常飲食＋注射 CCl4 、 CCl4 ＋一倍 (1×) 劑量組 (1×HE
，分別添加枸杞地黃熱水萃取物各 0.05% (w/w) 於飼料中 ) 、 CCl4 ＋三倍 (3×) 劑量 組 (3×HE ，分別添加枸杞地黃熱水萃取物各 0.15% (w/w) 於飼料中 ) 。一倍劑量與三 倍劑量組於誘發肝傷害前一週即開始給予枸杞地黃熱水萃取物，之後每週注射一次 CCl 4 ，實驗為期八週。結果顯示給予枸杞地黃熱水萃取物一週後，可顯著降低血漿三酸甘 油酯。八週期間，ㄧ倍與三倍劑量均可顯著降低血漿 GOT 、 GPT 活性與三酸甘油酯含 量，且三倍劑量可降低肝臟總膽固醇濃度。病理切片結果顯示一倍與三倍劑量均可抑制 由 CCl4 所造成肝細胞壞死、發炎細胞聚集與纖維化之情形。在發炎反應方面一倍與三 倍劑量均可抑制肝臟中 tumor necrosis factor-α (TNF-α) 、 interleukin-1 (IL-1β) 含量，一 倍劑量可提升肝臟中抗發炎細胞激素 interleukin-10 (IL-10) 之含量。且一倍與三倍劑量 具抑制肝臟導致纖維化的重要因子 transforming growth factor-β1 (TGF-β1) 之含量的功能
，且可減少肝臟中膠原蛋白之前驅物羥基脯胺酸 (hydroxyproline) 含量，對於肝纖維化 具有抑制的功能。但血漿總膽固醇含量、肝臟中脂肪堆積與三酸甘油酯含量、總抗氧化 狀態與脂質過氧化產物無差異。因此，給予枸杞地黃熱水萃取物可降低四氯化碳誘發肝 傷害老鼠血漿 GOT 、 GPT 活性，並藉由降低發炎反應，達到抑制肝臟損傷及纖維化之 功能。
Effect of hot water extracted Lycium barbarum and Rehmannia glutinosa on carbon tetrachloride-induced liver injury in rats
This study investigated the effects of hot water extracted Lycium barbarum and Rehmannia gl utinosa (HE) on hepato- pathological examination, liver functions, lipid metabolism, antioxida tive function, as well as inflammation and fibrosis in male Sprague Dawley rats with carbon te trachloride (CCl4)-induced liver injury. Rats (n = 10 per group) were randomly divided into: n ormal diet + peritoneal injection of olive oil (normal), normal diet+CCl4 injection (CCl4), 1 HE (0.05% HE for each)+CCl4 (1? HE), and 3 HE (0.15% HE for each)+CCl4 (3? HE) grou ps. Hot water extracted Lycium barbarum and Rehmannia glutinosa were given in the 1 HE a nd 3 HE groups a week prior to the induction of liver injury. Rats were injected with CCl4 o nce a week for 7 weeks. The results showed that plasma triglycerides decreased significantly a fter rats were given HE for one week. Both 1 and 3 HE treatments for 8 weeks decreased n ot only plasma GOT and GPT activities, but also triglyceride contents. The 3 HE treatment r educed liver cholesterol contents. The pathological examination showed both 1 and 3 HE d iminished necrotic hepatocytes, chemoattraction of inflammation cells, and fibrosis. Both 1 a nd 3 HE treatments reduced tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1β) . The 1? HE treatment increased interleukin-10 (IL-10) contents. Both 1? and 3? HE treatments supp ressed transforming growth factor-β1 (TGF-β1) concentraction. However, HE did not affect pl asma cholesterol, hepatic fat accumulation, hepatic total antioxidant status, and lipid peroxides . Therefore, HE can decrease CCl4-induced liver injury rats plasma GOT and GPT activitie s, and prevent liver injury and fibrosis by down-regulation of inflammation.
