Bang Byoung Wook, Park Dongsun, Kwon Kye Sook, Lee Don Haeng, Jang Min-Jung, Park Sun Kyu, Kim Jeom-Yong
1 Division of Gastroenterology, Department of Internal Medicine, Inha University College of Medicine, Incheon, South Korea.
2 Department of Biology Education, Korea National University of Education, Cheongju, South Korea.
J Med Food. 2019 Feb;22(2):140-151. doi: 10.1089/jmf.2018.4231. Epub 2019 Jan 24.
The gastroprotective effects of BST-104 (a water extract of Lonicera japonica) and the mechanisms involved were investigated in murine models of gastritis and peptic ulcer. The gastroprotective effects of BST-104 and its active components were evaluated in rat models of HCl/ethanol-induced gastritis and acetic acid-induced gastric ulcer. After orally administering BST-104, chlorogenic acid, rebamipide (positive control), or vehicle to each animal model, gastric lesion sizes, gastric mucus statuses, proinflammatory cytokine levels, and oxidative stress were measured. Superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) levels and oxidized/reduced glutathione (GSH) ratios in gastric mucosal tissues were measured to evaluate oxidative stress. To clarify the action mechanism of BST-104, we investigated nuclear factor (NF)-κB pathway involvement by real-time polymerase chain reaction (PCR). In the acetic acid-induced ulcer model, oral administration of BST-104 at 50, 100, or 200 mg/kg significantly reduced gastric lesions by 38%, 43%, and 55%, respectively, compared with vehicle controls. BST-104 significantly increased gastric mucus contents and this was accompanied by higher levels of hexosamine, sialic acid, and prostaglandin E in gastric mucus. Furthermore, BST-104 treatment increased antioxidant activities, as evidenced by higher levels of catalase, SOD, and oxidized/reduced GSH and lower MDA levels. In addition, BST-104 significantly suppressed proinflammatory cytokine (tumor necrosis factor-α, interleukin [IL]-6, and IL-1β) increases, and real-time PCR showed that BST-104 significantly downregulated NF-κB expression. In summary, BST-104 and its active component, chlorogenic acid, were found to have gastroprotective effects by virtue of their antioxidant and anti-inflammatory properties through downregulation of NF-κB expression.
在胃炎和消化性溃疡的小鼠模型中研究了BST-104（忍冬水提取物）的胃保护作用及其相关机制。在盐酸/乙醇诱导的胃炎和乙酸诱导的胃溃疡大鼠模型中评估了BST-104及其活性成分的胃保护作用。给每个动物模型口服BST-104、绿原酸、瑞巴派特（阳性对照）或赋形剂后，测量胃损伤大小、胃黏液状态、促炎细胞因子水平和氧化应激。测量胃黏膜组织中的超氧化物歧化酶（SOD）、过氧化氢酶和丙二醛（MDA）水平以及氧化型/还原型谷胱甘肽（GSH）比率以评估氧化应激。为阐明BST-104的作用机制，我们通过实时聚合酶链反应（PCR）研究了核因子（NF）-κB途径的参与情况。在乙酸诱导的溃疡模型中，与赋形剂对照组相比，口服50、100或200mg/kg的BST-104可使胃损伤分别显著减少38%、43%和55%。BST-104显著增加胃黏液含量，同时胃黏液中的氨基葡萄糖、唾液酸和前列腺素E水平升高。此外，BST-104治疗增加了抗氧化活性，表现为过氧化氢酶、SOD水平升高以及氧化型/还原型GSH升高和MDA水平降低。此外，BST-104显著抑制促炎细胞因子（肿瘤坏死因子-α、白细胞介素[IL]-6和IL-1β）的增加，实时PCR显示BST-104显著下调NF-κB表达。总之，发现BST-104及其活性成分绿原酸通过下调NF-κB表达，凭借其抗氧化和抗炎特性具有胃保护作用。
