Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University, Changchun 130118, China.
School of Life Sciences, Jilin University, Changchun 130012, China.
Oxid Med Cell Longev. 2020 Jan 8;2020:4054520. doi: 10.1155/2020/4054520. eCollection 2020.
(AM), which is rich in anthocyanins and procyanidins, has been reported to exert antioxidative and anti-inflammatory effects. This study aimed to systematically analyze the components of AM and explore its effects on alcohol-induced chronic liver injury in mice. A component analysis of AM revealed 17 types of fatty acids, 17 types of amino acids, 8 types of minerals, and 3 types of nucleotides. Chronic alcohol-induced liver injury was established in mice via gradient alcohol feeding over a period of 6 months, with test groups orally receiving AM in the last 6 weeks. AM administration yielded potential hepatoprotective effects by alleviating weight gain and changes in organ indexes, decreasing the ratio of alanine aminotransferase/aspartate aminotransferase, reducing lipid peroxidation, enhancing antioxidant activities, decreasing oxidation-related factor levels, and regulating inflammatory cytokine levels. Histological analyses suggest that AM treatment markedly prevented organ damage in alcohol-exposed mice. Furthermore, AM activated nuclear factor erythroid 2-like 2 (Nrf2) by downregulating the expression of Kelch-like ECH-associated protein 1, resulting in elevated downstream antioxidative enzyme levels. AM activated Nrf2 via modulation of the phosphatidylinositol-3-hydroxykinase/protein kinase B signaling pathway. Altogether, AM prevented alcohol-induced liver injury, potentially by suppressing oxidative stress via the Nrf2 signaling pathway.
（AM）富含花青素和原花青素，已被报道具有抗氧化和抗炎作用。本研究旨在系统分析 AM 的成分，并探索其对酒精诱导的小鼠慢性肝损伤的影响。AM 的成分分析显示含有 17 种脂肪酸、17 种氨基酸、8 种矿物质和 3 种核苷酸。通过梯度酒精喂养 6 个月在小鼠中建立慢性酒精性肝损伤，实验组在最后 6 周口服 AM。AM 通过减轻体重增加和器官指数变化、降低丙氨酸氨基转移酶/天冬氨酸氨基转移酶比值、减少脂质过氧化、增强抗氧化活性、降低氧化相关因子水平和调节炎症细胞因子水平，对酒精诱导的肝损伤产生潜在的保护作用。组织学分析表明，AM 治疗显著预防了酒精暴露小鼠的器官损伤。此外，AM 通过下调 Kelch 样 ECH 相关蛋白 1 的表达激活核因子红细胞 2 样 2（Nrf2），从而提高下游抗氧化酶水平。AM 通过调节磷脂酰肌醇-3-羟激酶/蛋白激酶 B 信号通路激活 Nrf2。总之，AM 通过 Nrf2 信号通路抑制氧化应激来预防酒精性肝损伤。
