文献类型：期刊文献

英文题名：Kaempferol protects ethanol-induced gastric ulcers in mice via pro-inflammatory cytokines and NO

作者：Li, Qinchen[1];Hu, Xinxin[1];Xuan, Yanhan[1];Ying, Jianghua[1];Fei, Yujia[1];Rong, Jielu[1];Zhang, Yong[1];Zhang, Jian[2];Liu, Chunyan[3];Liu, Zheng[1,2]

机构：[1]Shaoxing Univ, Dept Forens Toxicol, Judicial Identificat Ctr, Shaoxing 312000, Peoples R China;[2]Shaoxing Univ, Dept Pharmacolgoy, Coll Med, Shaoxing 312000, Peoples R China;[3]Shaoxing Peoples Hosp, Dept Orthopaed, Shaoxing 312000, Peoples R China

年份：2018

卷号：50

期号：3

起止页码：246

外文期刊名：ACTA BIOCHIMICA ET BIOPHYSICA SINICA

收录：SCI-EXPANDED(收录号：WOS:000428388600003)、、Scopus(收录号：2-s2.0-85044654578)、WOS

基金：This work was surppoted by the grants from the Public Welfare Technology Applied Research Projects in Zhejiang Province, China (No. 2016C33191), Zhejiang Provincial Natural Science Foundation of China (No. LY16C090003), the Science & Technology Planning Project of Shaoxing City, China (No. 2014B70052), and the Scientific Research Fund of Shaoxing University (No. 20125025).

语种：英文

外文关键词：ethanol; gastric ulcer; kaempferol; anti-inflammatory cytokine; NO

外文摘要：Gastric ulcers (GUs) are common pathologies that affect many people around the world. Excessive alcohol consumption is one of the main causes of GUs; however, there are still lack of effective drugs for the prevention or therapy of GUs. In this study, we evaluated the protective effects and possible mechanisms of kaempferol (KAE) against acute ethanol-induced lesions to the gastric mucosa in mice. Fasted mice were orally given vehicle (0.9% saline), omeprazole (20 mg/kg), or KAE (40, 80, or 160 mg/kg) for 1 h in different experimental sets prior to the establishment of the GU model by challenge with absolute ethanol (10 ml/kg). Animals were euthanized 1 h after ethanol intake, and their plasma and stomach tissues were subject to further examination. Macroscopic and microscopic lesions, and immunological and biochemical parameters were observed. The effects of inflammation were investigated using the following indicators: tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, myeloperoxidase (MPO), and nitric oxide (NO). Results showed that KAE significantly decreased the ulcer index, increased the preventive index, completely protected the mucosa from lesions, and preserved gastric mucosal glycoprotein. KAE decreased MPO activity and pro-inflammatory cytokine (TNF-alpha, and IL-1 beta) levels, and improved NO levels. The gastroprotective activity of KAE might be attributed to the preservation of gastric mucous glycoproteins levels, thus by inhibiting neutrophil accumulation and MPO activity, adjusting the levels of pro-inflammatory cytokines, and improving NO production.