Chang Hsin-Fang, Lin Yun-Ho, Chu Chia-Chou, Wu Shu-Ju, Tsai Ya-Hui, Chao Jane C-J
School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, Taiwan.
Am J Chin Med. 2007;35(6):995-1009. doi: 10.1142/S0192415X07005466.
This study investigated the effects of the combined extracts of Ginkgo biloba, Panax ginseng, and Schizandra chinensis at different doses on hepatic antioxidant status and fibrosis in rats with carbon tetrachloride (CCl4)-induced liver injury. Male Sprague-Dawley rats (n = 8-12 per group) were divided into the control, CCl4, CCl4 + silymarin (0.35%), CCl4 + low-dose herbal extract (0.24% of Ginkgo biloba, Panax ginseng, and Schizandra chinensis extract at 1:1:1; LE), and CCl4 + high-dose herbal extract (1.20% of the same herbal extract; HE) groups. Silymarin or herbal extract was orally given to rats a week before chronic intraperitoneal injection with CCl4 for 6 weeks. The pathological results showed that herbal extract suppressed hepatic bile duct proliferation, and low-dose herbal extract inhibited liver fibrosis. Hepatic superoxide dismutase (SOD) activity was lower in the CCl4 group, but there was no difference in the silymarin or herbal extract treated groups compared to the control group. Hepatic catalase activity and the ratio of reduced to oxidized glutathione were significantly higher (p < 0.05) in the HE group than those in the CCl4 group. Silymarin and herbal extract reversed the impaired hepatic total antioxidant status (p < 0.05). Herbal extract partially reduced the elevated hepatic lipid peroxides. Hepatic transforming growth factor-beta1 (TGF-beta1) level decreased significantly (p < 0.05) in the LE group. Therefore, high-dose herbal extract improved hepatic antioxidant capacity through enhancing catalase activity and glutathione redox status, whereas low-dose herbal extract inhibited liver fibrosis through decreasing hepatic TGF-beta1 level in rats with CCl4-induced liver injury.
本研究调查了不同剂量的银杏叶、人参和五味子联合提取物对四氯化碳(CCl4)诱导的肝损伤大鼠肝脏抗氧化状态和纤维化的影响。将雄性Sprague-Dawley大鼠(每组n = 8 - 12只)分为对照组、CCl4组、CCl4 + 水飞蓟宾(0.35%)组、CCl4 + 低剂量草药提取物组(银杏叶、人参和五味子提取物按1:1:1比例,0.24%;LE)和CCl4 + 高剂量草药提取物组(相同草药提取物1.20%;HE)。在慢性腹腔注射CCl4 6周前一周,给大鼠口服水飞蓟宾或草药提取物。病理结果显示,草药提取物抑制肝胆管增生,低剂量草药提取物抑制肝纤维化。CCl4组肝脏超氧化物歧化酶(SOD)活性较低,但与对照组相比,水飞蓟宾或草药提取物处理组无差异。HE组肝脏过氧化氢酶活性以及还原型谷胱甘肽与氧化型谷胱甘肽的比值显著高于CCl4组(p < 0.05)。水飞蓟宾和草药提取物逆转了受损的肝脏总抗氧化状态(p < 0.05)。草药提取物部分降低了升高的肝脏脂质过氧化物。LE组肝脏转化生长因子-β1(TGF-β1)水平显著降低(p < 0.05)。因此,高剂量草药提取物通过增强过氧化氢酶活性和谷胱甘肽氧化还原状态改善肝脏抗氧化能力,而低剂量草药提取物通过降低CCl4诱导的肝损伤大鼠肝脏TGF-β1水平抑制肝纤维化。