Chu C Y, Tseng T H, Hwang J M, Chou F P, Wang C J
Institute of Biochemistry, Chung Shan Medical and Dental College, Taichung, Taiwan, Republic of China.
Arch Toxicol. 1999 Jun-Jul;73(4-5):263-8. doi: 10.1007/s002040050615.
Capillarisin (Cap), a main constituent of Artemisia capillaris (Compositae), was studied for its antioxidant bioactivity. In the preliminary study, Cap expressed a antioxidant property by its capacity for quenching the free radicals of 1,1-diphenyl-2-picrylhydrazyl (DPPH). This antioxidant bioactivity of Cap was investigated further using a model of t-butylhydroperoxide (t-BHP)-induced cytotoxicity and genotoxicity in rat primary hepatocytes. Results presented here demonstrate that Cap, at concentrations of 0.01-1.00 mg/ml, significantly decreased the leakage of lactate dehydrogenase (LDH) and alanine aminotransferase (ALT) and the formation of malondialdehyde (MDA) induced by 30 min treatment of t-BHP (1.5 mM) in primary cultured rat hepatocytes. Cap also attenuated the t-BHP-induced diminution of glutathione (GSH) and high level of DNA repaired synthesis. These results lead to speculation that Cap presents inhibitory effects against t-BHP-caused cytotoxicity and genotoxicity in rat primary hepatocyte cultures at least via two distinct pathways, stabilizing the GSH system and quenching free radicals.
茵陈色原酮（Cap）是茵陈蒿（菊科）的主要成分，对其抗氧化生物活性进行了研究。在初步研究中，Cap通过淬灭1,1-二苯基-2-苦基肼（DPPH）自由基的能力表现出抗氧化特性。使用叔丁基过氧化氢（t-BHP）诱导大鼠原代肝细胞细胞毒性和遗传毒性的模型进一步研究了Cap的这种抗氧化生物活性。此处给出的结果表明，在0.01 - 1.00 mg/ml浓度下，Cap显著降低了原代培养大鼠肝细胞经30分钟1.5 mM t-BHP处理后诱导的乳酸脱氢酶（LDH）和丙氨酸转氨酶（ALT）泄漏以及丙二醛（MDA）的形成。Cap还减弱了t-BHP诱导的谷胱甘肽（GSH）减少和高水平的DNA修复合成。这些结果引发推测，Cap至少通过两种不同途径对大鼠原代肝细胞培养物中t-BHP引起的细胞毒性和遗传毒性具有抑制作用，即稳定GSH系统和淬灭自由基。
