Department of Internal Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea.
Life Science R&D Center, SK Chemicals, Suwon, Korea.
Gut Liver. 2014 Jan;8(1):49-57. doi: 10.5009/gnl.2014.8.1.49. Epub 2013 Nov 5.
BACKGROUND/AIMS: The major compounds of Cochinchina momordica seed extract (SK-MS10) include momordica saponins. We report that the gastroprotective effect of SK-MS10 in an ethanol-induced gastric damage rat model is mediated by suppressing proinflammatory cytokines and downregulating cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase (5-LOX), and the activation of calcitonin gene-related peptide. In this study, we evaluated the gastroprotective effects of SK-MS10 in the nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage rat model.
The pretreatment effect of SK-MS10 was evaluated in the NSAID-induced gastric damage rat model using aspirin, indomethacin, and diclofenac in 7-week-old rats. Gastric damage was evaluated based on the gross ulcer index by gastroenterologists, and the damage area (%) was measured using the MetaMorph 7.0 video image analysis system. Myeloperoxidase (MPO) was measured by enzyme-linked immunosorbent assay, and Western blotting was used to analyze the levels of cyclooxygenase (COX)-1, COX-2, cPLA2, and 5-LOX.
All NSAIDs induced gastric damage based on the gross ulcer index and damage area (p<0.05). Gastric damage was significantly attenuated by SK-MS10 pretreatment compared with NSAID treatment alone (p<0.05). The SK-MS10 pretreatment group exhibited lower MPO levels than the diclofenac group. The expression of cPLA2 and 5-LOX was decreased by SK-MS10 pretreatment in each of the three NSAID treatment groups.
SK-MS10 exhibited a gastroprotective effect against NSAID-induced acute gastric damage in rats. However, its protective mechanism may be different across the three types of NSAID-induced gastric damage models in rats.
背景/目的:越南苦瓜种子提取物(SK-MS10)的主要化合物包括苦瓜皂甙。我们报告说,SK-MS10 在乙醇诱导的胃损伤大鼠模型中的胃保护作用是通过抑制促炎细胞因子和下调细胞质磷脂酶 A2(cPLA2)、5-脂氧合酶(5-LOX)以及降钙素基因相关肽的激活来介导的。在这项研究中,我们评估了 SK-MS10 在非甾体抗炎药(NSAID)诱导的胃损伤大鼠模型中的胃保护作用。
使用阿司匹林、吲哚美辛和双氯芬酸在 7 周龄大鼠中评估 SK-MS10 在 NSAID 诱导的胃损伤大鼠模型中的预处理作用。根据胃肠病学家的大体溃疡指数评估胃损伤,并用 MetaMorph 7.0 视频图像分析系统测量损伤面积(%)。通过酶联免疫吸附试验测量髓过氧化物酶(MPO),并用 Western blot 分析环加氧酶(COX)-1、COX-2、cPLA2 和 5-LOX 的水平。
所有 NSAID 均基于大体溃疡指数和损伤面积诱导胃损伤(p<0.05)。与 NSAID 单独治疗相比,SK-MS10 预处理显着减轻了胃损伤(p<0.05)。与双氯芬酸组相比,SK-MS10 预处理组的 MPO 水平较低。在三种 NSAID 治疗组中,SK-MS10 预处理均降低了 cPLA2 和 5-LOX 的表达。
SK-MS10 对大鼠 NSAID 诱导的急性胃损伤表现出胃保护作用。然而,其保护机制在三种类型的 NSAID 诱导的大鼠胃损伤模型中可能不同。