Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, College of Pharmacy, China Medical University, Taichung 404, Taiwan.
Food Chem. 2013 Dec 1;141(3):3020-7. doi: 10.1016/j.foodchem.2013.03.061. Epub 2013 Apr 6.
The hepatoprotective effects of eburicoic acid (TR1) and dehydroeburicoic acid (TR2) from Antrodia camphorata (AC) against carbon tetrachloride (CCl4)-induced liver damage were investigated in mice. TR1 and TR2 was administered intraperitoneally (i.p.) for 7 days prior to the administration of CCl4. Pretreatment with TR1 and TR2 prevented the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and liver lipid peroxides in CCl4-treated mice. The activities of antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx)], nitric oxide (NO) production, and tumour necrosis factor-alpha (TNF-α) were decreased after the treatment with TR1 and TR2 in CCl4-treated mice. Western blotting revealed that TR1 and TR2 significantly decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expressions and increased the expression of cytochrome P4502E1 (CYP2E1) in CCl4-treated mice. Therefore, we speculate that TR1 and TR2 protect the liver from CCl4-induced hepatic damage via antioxidant and anti-inflammatory mechanisms.
从牛樟芝(Antrodia camphorata,AC)中分离得到的 7,8-去氢辛二酸(TR1)和辛二酸(TR2)对四氯化碳(CCl4)诱导的肝损伤的保护作用进行了研究。在给予 CCl4 之前,TR1 和 TR2 通过腹腔内给药(i.p.)给药 7 天。TR1 和 TR2 预处理可防止 CCl4 处理小鼠天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)和肝脂质过氧化物的升高。TR1 和 TR2 处理可降低 CCl4 处理小鼠的抗氧化酶[过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)]、一氧化氮(NO)产生和肿瘤坏死因子-α(TNF-α)的活性。Western blot 分析表明,TR1 和 TR2 可显著降低诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的表达,并增加 CCl4 处理小鼠细胞色素 P4502E1(CYP2E1)的表达。因此,我们推测 TR1 和 TR2 通过抗氧化和抗炎机制保护肝脏免受 CCl4 诱导的肝损伤。