Excessive alcohol consumption causes liver injury–induced mortality. Here we systematically analyzed the structure of triterpenoids extracted from Antrodia cinnamomea mycelia (ACT) and investigated their protective effects against acute alcohol-induced liver injury in mice. Liquid chromatography–mass spectrometry and liquid chromatography with tandem mass spectrometry were performed to determine the structures of ACT constituents. Alcohol-induced liver injury was generated in C57BL/6 mice by oral gavage of 13 g/kg white spirit (a wine at 56% ABV). Mice were treated with either silibinin or ACT for 2 weeks. Liver injury markers and pathological signaling were then quantified with enzyme-linked immunosorbent assays, antibody array assays, and Western blots, and pathological examinations were performed using hematoxylin-eosin staining and periodic acid–Schiff staining. Triterpenoids extracted from A. cinnamomea mycelia contain 25 types of triterpenoid compounds. A 2-weeks alcohol consumption treatment caused significant weight loss, liver dyslipidemia, and elevation of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transferase, and alkaline phosphatase activities in the serum and/or liver. These effects were markedly reversed after 2-weeks ACT administration. Triterpenoids extracted from A. cinnamomea mycelia alleviated the organ structural changes and inflammatory infiltration of alcohol-damaged tissues. Triterpenoids extracted from A. cinnamomea mycelia inhibited proinflammatory cytokine levels and enhanced anti-inflammatory cytokine levels. Acute alcohol treatment promoted inflammation with significant correlations to hypoxia-inducible factor 1α (HIF-1α), which was reduced by ACT and was partially related to modulation of the protein kinase B (Akt)/70-kDa ribosomal protein S6 kinase phosphorylation (p70S6K) and Wnt/β-catenin signaling pathways. In conclusion, ACT protected against acute alcohol-induced liver damage in mice mainly through its suppression of the inflammatory response, which may be related to HIF-1α signaling.

过量饮酒会导致肝损伤而导致死亡。在这里，我们系统地分析了从中提取的三萜类化合物的结构。肉桂牛樟芝菌丝体（ACT）并研究了它们对小鼠急性酒精性肝损伤的保护作用。进行了液相色谱-质谱和串联质谱液相色谱法来确定ACT成分的结构。通过口服管饲13 g / kg的白酒（56％ABV的葡萄酒），在C57BL / 6小鼠中产生了酒精诱导的肝损伤。用水飞蓟宾或ACT治疗小鼠2周。然后通过酶联免疫吸附测定，抗体阵列测定和Western印迹对肝损伤标记物和病理信号进行定量，并使用苏木精-伊红染色和高碘酸-席夫氏染色进行病理检查。从中提取的三萜肉桂菌丝体含有25种三萜类化合物。饮酒2周的治疗导致体重减轻，肝脏血脂异常以及血清和/或肝脏中丙氨酸氨基转移酶，天冬氨酸氨基转移酶，γ-谷氨酰转移酶和碱性磷酸酶活性的升高。ACT治疗2周后，这些作用明显逆转。从中提取的三萜肉桂菌丝体减轻了酒精损伤组织的器官结构变化和炎症浸润。从中提取的三萜肉桂菌丝体抑制促炎细胞因子水平并增强抗炎细胞因子水平。急性酒精治疗可促进炎症，与低氧诱导因子1α（HIF-1α）具有显着相关性，后者可通过ACT降低，部分与蛋白激酶B（Akt）/ 70-kDa核糖体蛋白S6激酶磷酸化（p70S6K）的调节有关）和Wnt /β-catenin信号通路。总之，ACT主要通过抑制炎症反应来预防小鼠急性酒精性肝损伤，这可能与HIF-1α信号传导有关。