Zhou Tiantian, Mao Xue, Jiang Wei, Pan Yu, Chen Xijun, Hu Jihua, Kong Xianghui, Xia Haihua
Institute of Microbiology, Heilongjiang Academy of Sciences, Harbin, China.
Key Laboratory of Flexible Electronics, Institute of Advanced Materials, Nanjing Tech University, Nanjing, China.
Front Nutr. 2023 Jun 12;10:1161537. doi: 10.3389/fnut.2023.1161537. eCollection 2023.
Non-alcoholic fatty acid liver disease (NAFLD) is a reputed global health concern, affecting children and young adults. Accumulating evidence suggests that edible fungi polysaccharides have the potential to relieve NAFLD. Our previous study found that var. Li. polysaccharides (ACP) could improve immune by regulating gut microbiota. However, its NAFLD-alleviating potentials have been scarcely reported. This study analyzed the protective effects of var. Li. polysaccharides on high-fat diet (HFD)-induced NAFLD and mechanistic actions. We first analyzed the histology and hepatic lipid profile of animals to evaluate this variant's ameliorating effects on NAFLD. Then, antioxidant and anti-inflammatory potentials of ACP were studied. Finally, we explored changes in the gut microbiome diversity for mechanistic insights from the gut-liver region. Results showed that supplementation with ACP substantially reduced homeostasis model assessment-insulin resistance (HOMA-IR), body fat, liver index rates and weight gain ( < 0.05). This variant also improved HDL-C levels while decreasing triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels which were initially triggered by HFD. ACP mediation also decreased the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels considerably with H&E technique indicating that it can reduce liver lipid accumulation, thus lowering liver damages risks ( < 0.05). The antioxidant potentials of ACP were also demonstrated as it decreased the hepatic levels of malondialdehyde (MDA) and increased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX). Proinflammatory markers like IL-6, IL-1β and TNF-α concentrations were decreased by ACP supplementation, accompanied with increased IL-4 levels. Finally, ACP supplementation regulated the intestinal microbiota to near normal patterns. In all, ACP protects HFD-induced NAFLD by improving liver characteristics and regulating colonic flora composition, our findings assert that ACP can be a promising strategy in NAFLD therapy.
非酒精性脂肪性肝病（NAFLD）是一个备受关注的全球性健康问题，影响着儿童和年轻人。越来越多的证据表明，食用真菌多糖有可能缓解NAFLD。我们之前的研究发现，香菇多糖（ACP）可以通过调节肠道微生物群来增强免疫力。然而，其减轻NAFLD的潜力鲜有报道。本研究分析了香菇多糖对高脂饮食（HFD）诱导的NAFLD的保护作用及其作用机制。我们首先分析了动物的组织学和肝脏脂质谱，以评估该变体对NAFLD的改善作用。然后，研究了ACP的抗氧化和抗炎潜力。最后，我们探索了肠道微生物群多样性的变化，以从肠-肝区域获得机制性见解。结果表明，补充ACP可显著降低稳态模型评估-胰岛素抵抗（HOMA-IR）、体脂、肝脏指数率和体重增加（<0.05）。该变体还提高了高密度脂蛋白胆固醇（HDL-C）水平，同时降低了最初由HFD引发的甘油三酯（TG）、总胆固醇（TC）和低密度脂蛋白胆固醇（LDL-C）水平。ACP的调节作用还显著降低了血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）水平，苏木精-伊红（H&E）染色技术表明它可以减少肝脏脂质积累，从而降低肝损伤风险（<0.05）。ACP的抗氧化潜力也得到了证明，因为它降低了肝脏丙二醛（MDA）水平，并提高了超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-PX）的活性。补充ACP可降低促炎标志物如白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）的浓度，并伴有白细胞介素-4（IL-4）水平升高。最后，补充ACP将肠道微生物群调节至接近正常模式。总之，ACP通过改善肝脏特征和调节结肠菌群组成来保护HFD诱导的NAFLD，我们的研究结果表明，ACP可能是NAFLD治疗中的一种有前景的策略。
