Niu-Chang-Chih · 2003 · Research Support, Non U.S. Gov'T
Medium relevanceAntioxidative and hepatoprotective effects of Antrodia camphorata extract.
Antrodia camphorata
Key points
- The purpose of this study was to evaluate the ability of A. camphorata extracts to protect against oxidative stress in vitro and against carbon tetrachloride (CCl(4))-induced hepatic injury in vivo
- An extract of A. camphorata inhibited nonenzymatic iron-induced lipid peroxidation in rat brain homogenates with an IC(50) value about 3.1 mg/mL. It also scavenged the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH)
- The dose of the A. camphorata extract resulting in a decrease of 0.20 in the absorbance of DPPH was about 31 +/- 0.7 microg/mL. Furthermore, an A. camphorata extract dose-dependently (250-1250 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated CCl(4) intoxication in mice
- Moreover, A. camphorata extract significantly improved the CCl(4)-induced increase in hepatic glutathione peroxidase, reductase, and CCl(4)-induced decrease in superoxide dismutase activities
- Furthermore, it also dose-dependently inhibited the formation of lipid peroxidative products during CCl(4) treatment
- Histopathological changes of hepatic lesions induced by CCl(4) were significantly ameliorated by treatment with an A. camphorata extract in a dose-dependent manner
Metadata-grounded summary
Citation abstract
Antrodia camphorata (A. camphorata) is well-known in Taiwan as a traditional Chinese medicine. The purpose of this study was to evaluate the ability of A. camphorata extracts to protect against oxidative stress in vitro and against carbon tetrachloride (CCl(4))-induced hepatic injury in vivo. An extract of A. camphorata inhibited nonenzymatic iron-induced lipid peroxidation in rat brain homogenates with an IC(50) value about 3.1 mg/mL. It also scavenged the stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH). The dose of the A. camphorata extract resulting in a decrease of 0.20 in the absorbance of DPPH was about 31 +/- 0.7 microg/mL. Furthermore, an A. camphorata extract dose-dependently (250-1250 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated CCl(4) intoxication in mice. Moreover, A. camphorata extract significantly improved the CCl(4)-induced increase in hepatic glutathione peroxidase, reductase, and CCl(4)-induced decrease in superoxide dismutase activities. It also restored the decrement in the glutathione content and catalase activity of hepatic tissues in CCl(4)-intoxicated mice. Furthermore, it also dose-dependently inhibited the formation of lipid peroxidative products during CCl(4) treatment. Histopathological changes of hepatic lesions induced by CCl(4) were significantly ameliorated by treatment with an A. camphorata extract in a dose-dependent manner. These results suggest that A. camphorata extract exerts effective protection against chronic chemical-induced hepatic injury in vivo, by mediating antioxidative and free radical scavenging activities.
Citation
Hsiao G, Shen MY, Lin KH, Lan MH, Wu LY, Chou DS, et al. (2003). Antioxidative and hepatoprotective effects of Antrodia camphorata extract. Journal of agricultural and food chemistry https://doi.org/10.1021/jf021159t PMID: 12744658
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