Wu, Min-TzeMin-TzeWuTzang, Bor-ShowBor-ShowTzangChang, Yuan-YenYuan-YenChangCHIH-HSIEN CHIUKang, Wen-YuWen-YuKangHuang, Chia-HsinChia-HsinHuangYI-CHEN CHEN2019-09-262019-09-262011-04-270021-85611520-5118https://scholars.lib.ntu.edu.tw/handle/123456789/425334Alcoholic fatty liver disease (AFLD) is the result of an excessive or chronic consumption of alcohol. Nine male Wistar rats per group were randomly assigned to one of the following drinking treatments: a 20% (w/w) alcohol solution (ALC); a 20% (w/w) alcohol solution cotreated with 0.25 g silymarin/kg BW/day; or a 20% (w/w) alcohol solution cotreated with 0.025 g Niuchangchih ( Antrodia camphorata )/kg BW/day for 4 weeks. Rats with cotreatments of silymarin or Niuchangchih had smaller (p < 0.05) relative liver size, less (p < 0.05) liver lipid accumulation, and lower (p < 0.05) liver damage indices [aspartate aminotransferase (AST) and alkaline phosphatase (ALP) values]. In the regulation of alcohol metabolism, the lower serum alcohol level was observed only in alcohol-fed rats supplemented with Niuchangchih. Meanwhile, cotreatment of silymarin or Niuchangchih increased (p < 0.05) CAT and ALDH activities but did not (p > 0.05) affect ADH and CYP2E1 expressions, which accelerate alcohol metabolism in the body. Additionally, neither silymarin nor Niuchangchih (p > 0.05) influenced serum/hepatic MMP-2 activities and NF-κB, AP1, and α-SMA gene expressions, but serum/hepatic MMP-9 activities and TNF-α, KLF-6, and TGF-β1 gene expressions of alcohol-fed rats were down-regulated (p < 0.05) by silymarin or Niuchangchih, which also could explain the lower liver damage observed in rats chronically fed alcohol.enalcoholic fatty liver; Antrodia camphorata; liver lipid accumulation; liver damage index; alcohol metabolism; fibrosisjournal article10.1021/jf104561h214011002-s2.0-79955029861WOS:000289613500096https://api.elsevier.com/content/abstract/scopus_id/79955029861