Abstract
Tiao He Yi Wei granule (DHYW), a traditional Chinese medicine, has been used for the treatment of gastric ulcer in clinical setting. The purpose of the present study was to investigate the possible effect of DHYW and explore the underlying mechanism against ethanol-induced gastric ulcer in mice. The model of ethanol-induced gastric ulcer in mice was induced by ethanol (0.2 mL/kg). Administration of DHYW at the doses of 250, 500 mg/kg body weight prior to the ethanol ingestion could effectively protect the stomach from ulceration. The gastric lesions were significantly ameliorated in the DHYW group compared with that in the model group. Treatment with DHYW markedly decreased the levels of interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α). In addition, DHYW treatment elevated myeloperoxidase (MPO) level in stomach, increased superoxide dismutase (SOD) activity, and decreased malonaldehyde (MDA) content in serum and stomach compared with those in the model group. DHYW significantly inhibited NF-κB pathway expressions in the gastric mucosa ulcer group. Taken together, DHYW exerted a gastroprotective effect against gastric ulceration and the underlying mechanism might be associated with NF-κB pathway.
Highlights
Peptic ulcer is one of the most pervasive gastrointestinal diseases which affect 4-5% people in the society [1]
The enzyme-linked immunosorbent assay (ELISA) kits for determination of IL-6, IL-1β, and tumor necrosis factor-α (TNF-α) were produced by BioLegend (San Diego, CA, USA)
Ethanol is widely acknowledged as an abused agent to gastric ulceration [13]
Summary
Peptic ulcer is one of the most pervasive gastrointestinal diseases which affect 4-5% people in the society [1]. The gastric ulcer is characterized by the reduction in blood flow, induction of oxidative stress, infiltration of neutrophils, and secretion of proinflammatory cytokines [2, 3]. A variety of factors such as Helicobacter pylori infection, alcohol consumption, smoking, excessive use of nonsteroidal antiinflammatory drugs (NSAIDs), and psychological and physiological stress contribute to gastric ulcer [4]. Alcohol consumption increased the risk for major upper gastrointestinal bleeding [5]. As alcohol is one of the major abused agents, the alcohol-induced peptic ulcer is the common disorder of the gastrointestinal tract [6]. The free NF-κB translocates into the nucleus and leads to the transcriptional activation of several proinflammatory mediators including TNF-α, IL-1β, and IL-6 [10]
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