Yang Suqin, Liu Gang, Xia Xiankun, Gan Dali, Xiang Shijian, Xiang Meixian
School of Pharmaceutical Sciences, South-Central Minzu University, Wuhan 430074, China.
Department of Pharmacy, Renmin Hospital of Wuhan University, Wuhan, China, 430060, Hubei, China.
Heliyon. 2024 Jan 11;10(2):e24339. doi: 10.1016/j.heliyon.2024.e24339. eCollection 2024 Jan 30.
α-Mangostin is a natural xanthone derivative isolated from (CA), commonly known as Lichuan black tea (LBT). The present study investigated the ameliorating effect and mechanism of α-mangostin on alcoholic gastric ulcers (GU) in rats. , α-mangostin relieved pathological symptoms. Moreover, α-mangostin regulated the activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) and nuclear factor κB (NF-κB)/NLR family pyrin domain containing 3 (NLRP3)/caspase-1 pathways. Reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were significantly decreased and IL-10 were increased, the microtubule-associated protein light chain 3 (LC3)-II/LC3-I ratio was increased, p62 protein expression was decreased, and inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) protein expression was down-regulated. The relevant mechanisms were validated using GSE-1 and RAW264.7 cells in an model. Furthermore, α-mangostin increased and abundance as well as propionic acid and butyric acid contents. Therefore, α-mangostin possesses antioxidant and anti-inflammatory properties, and remodels intestinal flora dysbiosis through mechanisms that may involve regulation of the Nrf2/HO-1 pathway and NF-κB/NLRP3/caspase-1 pathway. It also increases propionic acid and butyric acid contents. This study provides novel evidence regarding the use of α-mangostin for treating GU.
α-山竹黄酮是一种从[具体来源未提及，可能是文档前文提到的某种物质]中分离出的天然呫吨酮衍生物，该物质通常被称为利川红茶（LBT）。本研究调查了α-山竹黄酮对大鼠酒精性胃溃疡（GU）的改善作用及其机制。结果显示，α-山竹黄酮缓解了病理症状。此外，α-山竹黄酮调节了核因子（红系衍生2）样2（Nrf2）/血红素加氧酶1（HO-1）以及核因子κB（NF-κB）/含NLR家族pyrin结构域蛋白3（NLRP3）/半胱天冬酶-1通路的激活。活性氧（ROS）、肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）显著降低，而IL-10增加，微管相关蛋白轻链3（LC3）-II/LC3-I比值升高，p62蛋白表达降低，诱导型一氧化氮合酶（iNOS）和环氧化酶2（COX-2）蛋白表达下调。在一个模型中使用GSE-1和RAW264.7细胞验证了相关机制。此外，α-山竹黄酮增加了[具体物质未提及，可能是文档前文提到的某种物质]丰度以及丙酸和丁酸含量。因此，α-山竹黄酮具有抗氧化和抗炎特性，并通过可能涉及调节Nrf2/HO-1通路和NF-κB/NLRP3/半胱天冬酶-1通路的机制重塑肠道菌群失调。它还增加了丙酸和丁酸含量。本研究为使用α-山竹黄酮治疗GU提供了新的证据。
