Since the liver is mainly responsib

由于肝脏主要负责人类的代谢功能，因此它对药物和其他化学物质敏感，涵盖氧化应激，细胞凋亡和炎症21。众所周知，酒精性肝病中减弱的肝酶功能和代偿性胆汁分泌会增加未结合的胆红素，加速黄疸的发展22,23。此外，酒精诱导的脂肪肝是肝脏缺氧的常见原因，过多的活性氧会攻击线粒体的DNA和蛋白质24,25。肌浆网/内质网钙ATPase泵对氧化应激高度敏感，会异常释放内质网中的钙离子，从而加剧线粒体代谢紊乱26,27。作为天然的类黄酮，槲皮素具有与内质网应激和炎症相关的肝保护作用。它不仅可以激活PI3K / Akt通路，从而动态调节Ca2 +并降低炎症细胞因子（IL-6，TNF-α）的表达，而且可以阻断Jun N端激酶（JNK）28的活性并最终对细胞进行正向调节增殖并抑制凋亡过程29.酒精诱导的脂肪肝会增加肝纤维化，肝硬化和肝细胞癌的发生率30。由于黄疸是这些疾病的常见症状，我们推测银芝黄可以激活PI3K / Akt途径，调节炎症因子和Ca2 +，涉及ATP结合，线粒体有氧代谢，肝细胞膜的膜运输等。

由于肝脏主要负责人体的代谢功能，因此对药物和其他化学物质敏感，包括氧化应激、凋亡和炎症21。据了解，酒精性肝病中减减肝酶功能和补偿性胆汁分泌增加未分的胆红素，加速黄斑22，23的发展。此外，酒精诱发的脂肪肝是肝缺氧的常见原因，过量活性氧物种攻击线粒体DNA和蛋白质24，25。与氧化应激的高敏感性，沙原体/内质性神经质钙 ATPase 泵异常释放内质神经质的钙离子，加重线粒体代谢紊乱 26，27。作为一种天然黄酮类化合物，奎塞汀具有与内质性神经性应激和炎症有关的肝保护作用。它不仅能够激活PI3K/Akt通路，从而产生Ca2+的动态调节，减少炎症细胞因子（IL-6，TNF-α）的表达，而且能够阻断Jun N-终端激酶（JNK）28的活动，最终积极调节细胞增殖并抑制凋亡过程29。酒精引起的脂肪肝可增加肝纤维化、肝硬化和肝细胞癌的发病率30。由于黄斑是这些疾病的常见症状，我们推测银志黄可以激活PI3K/Akt通路，调节炎症因子和Ca2+，涉及ATP结合、线粒体有氧代谢、肝细胞膜膜传输等。

Since the liver is mainly responsible for the metabolic function of the human, it is sensitive to drugs and other chemicals, covering oxidative stress, apoptosis and inflammation 21. It is known that attenuated liver enzyme function and compensatory bile secretion in alcoholic liver diseases increase the unconjugated bilirubin, accelerating the development of jaundice 22,23. Moreover, alcohol-induced fatty liver is the common cause of liver hypoxia, and excessive reactive oxygen species attacks mitochondrial DNA and proteins 24,25. With high sensitivity to oxidative stress, sarcoplasmic/endoplasmic reticulum calcium ATPase pump abnormally releases calcium ions in endoplasmic reticulum which aggravates mitochondrial metabolic disorders 26,27. As a natural flavonoid, quercetin has hepatoprotective effect related to endoplasmic reticulum stress and inflammation. It can not only activate PI3K/Akt pathway resulting in dynamic regulation of Ca2+ and reduced expression of inflammatory cytokines (IL-6, TNF-α), but block the activities of Jun N-terminal kinase (JNK) 28 and finally positively regulate cell proliferation and inhibit apoptotic process 29. Fatty liver induced by alcohol enhances the incidence of the liver fibrosis, cirrhosis, and hepatocellular carcinoma 30. As jaundice is a common symptom of these diseases, we speculate that Yinzhihuang can activate PI3K/Akt pathway, regulating inflammatory factors and Ca2+, involving in ATP binding, mitochondrial aerobic metabolism, membrane transport of hepatocelluar membrane and so on.<br>