Xie Min, Chen Haihong, Nie Shaoping, Tong Wei, Yin Junyi, Xie Mingyong
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.
State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.
Chem Biol Interact. 2017 Jun 25;272:125-134. doi: 10.1016/j.cbi.2017.04.022. Epub 2017 Apr 27.
The present study aimed to investigate the gastroprotective effect of gamma-aminobutyric acid (GABA) on ethanol-induced gastric mucosal injury and gastric epithelial cells injury. Rats were divided into the control group, vehicle group and GABA-treated groups (10, 20 and 40 mg/kg/day). After GABA ingestion for 14 days, rats except the control group were given 1 mL pure ethanol by oral gavage in order to induce acute gastric mucosal lesion. The human gastric epithelial cell line GES-1 was incubated with GABA (100, 200 and 400 μM) for 24 h, followed by treatment with 8% ethanol for 3 h to induce cell injury. The results showed that GABA pretreatment significantly reduced gastric ulcer index in a dose-dependent manner. GABA pretreatment could not only remarkably restrain oxidative stress by increasing activities of superoxide dismutase and catalase as well as decreasing content of malondialdehyde both in gastric tissue and cells, but also significantly reduced pro-inflammatory factors (interleukin-6 and tumor necrosis factor α) levels in gastric tissue. In addition, significant augments of prostaglandin E and nitric oxide levels were observed in the gastric tissues of 40 mg/kg/d GABA treated group. In conclusion, the results in this study suggested that GABA could alleviate ethanol-induced gastric mucosal injury and gastric epithelial cells injury through the improvement of anti-inflammatory and anti-oxidant status, as well as the increase of PGE and NO levels.
本研究旨在探讨γ-氨基丁酸（GABA）对乙醇诱导的胃黏膜损伤和胃上皮细胞损伤的胃保护作用。将大鼠分为对照组、溶媒组和GABA处理组（10、20和40mg/kg/天）。在摄入GABA 14天后，除对照组外的大鼠通过口服灌胃给予1mL纯乙醇以诱导急性胃黏膜损伤。将人胃上皮细胞系GES-1与GABA（100、200和400μM）孵育24小时，然后用8%乙醇处理3小时以诱导细胞损伤。结果表明，GABA预处理以剂量依赖性方式显著降低胃溃疡指数。GABA预处理不仅可以通过增加胃组织和细胞中超氧化物歧化酶和过氧化氢酶的活性以及降低丙二醛含量来显著抑制氧化应激，还可以显著降低胃组织中促炎因子（白细胞介素-6和肿瘤坏死因子α）的水平。此外，在40mg/kg/d GABA处理组的胃组织中观察到前列腺素E和一氧化氮水平显著升高。总之，本研究结果表明，GABA可以通过改善抗炎和抗氧化状态以及增加PGE和NO水平来减轻乙醇诱导的胃黏膜损伤和胃上皮细胞损伤。
