Yin Hong, Cai Hui-Zhen, Wang Shao-Kang, Yang Li-Gang, Sun Gui-Ju
Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, China.
School of Public Health, Ningxia Medical University, Yinchuan 750004, China.
Chin J Nat Med. 2015 Jan;13(1):22-9. doi: 10.1016/S1875-5364(15)60003-6.
Non-steroidal anti-inflammatory drugs (NSAIDs) induce tissue damage and oxidative stress in animal models of stomach damage. In the present study, the protective effects of wheat peptides were evaluated in a NSAID-induced stomach damage model in rats. Different doses of wheat peptides or distilled water were administered daily by gavage for 30 days before the rat stomach damage model was established by administration of NSAIDs (aspirin and indomethacin) into the digestive tract twice. The treatment of wheat peptides decreased the NSAID-induced gastric epithelial cell degeneration and oxidative stress and NO levels in the rats. Wheat peptides significantly increased the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and decreased iNOS activity in stomach. The mRNA expression level of μ-opioid receptor was significantly decreased in wheat peptides-treated rats than that in in the control rats. The results suggest that NSAID drugs induced stomach damage in rats, wchih can be prevented by wheat peptides. The mechanisms for the protective effects were most likely through reducing NSAID-induced oxidative stress.
非甾体抗炎药（NSAIDs）在胃损伤动物模型中会引发组织损伤和氧化应激。在本研究中，我们在NSAID诱导的大鼠胃损伤模型中评估了小麦肽的保护作用。在通过向消化道两次给予NSAIDs（阿司匹林和吲哚美辛）建立大鼠胃损伤模型之前，每天通过灌胃给予不同剂量的小麦肽或蒸馏水，持续30天。小麦肽治疗降低了NSAIDs诱导的大鼠胃上皮细胞变性、氧化应激和NO水平。小麦肽显著提高了胃中超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的活性，并降低了诱导型一氧化氮合酶（iNOS）的活性。与对照大鼠相比，经小麦肽处理的大鼠中μ-阿片受体的mRNA表达水平显著降低。结果表明，NSAID药物会诱导大鼠胃损伤，而小麦肽可以预防这种损伤。其保护作用的机制很可能是通过减轻NSAID诱导的氧化应激。
