Abstract
Ginger (Zingiber officianale), the most widely consumed species, is traditionally used as a folk medicine to treat some inflammatory diseases in China and Korea. However, the functional activity of steamed ginger extract on gastric ulcers has not been previously explored. The present study aimed to investigate antiulcer activity of steamed ginger extract (GGE03) against ethanol (EtOH)/HCl-induced gastric ulcers in a rat model. GGE03 (100 mg/kg) was orally administered for 14 days to rats before oral intubation of an EtOH/HCl mixture to induce gastric damage. Pretreatment with GGE03 markedly protected the formation of microscopic pathological damage in the gastric mucosa. Further, administration of GGE03 significantly increased mucosal total nitrate/nitrite production in gastric tissues, and elevated total GSH content, catalase activity and superoxide dismutase (SOD) expression as well as decreasing lipid peroxidation and myeloperoxidase (MPO) activity. Underlying protective mechanisms were examined by assessing inflammation-related genes, including nuclear factor-κB (NF-κB), prostaglandin E2 (PGE2), and pro-inflammatory cytokines levels. GGE03 administration significantly reduced the expression of NF-κB and pro-inflammatory cytokines. Our findings suggest that GGE03 possesses antiulcer activity by attenuating oxidative stress and inflammatory responses.
Highlights
Gastric ulcers are one of the most prevalent types of peptic ulcer commonly seen in humans, affecting more than 10% of the global population [1]
Our findings suggest that GGE03 possesses antiulcer activity by attenuating oxidative stress and inflammatory responses
The principal etiological factors associated with gastric ulcers are alcohol and non-steroidal anti-inflammatory drugs (NSAIDs) abuse, stress, smoking, and infection of H. pylori [2,3,4,5]
Summary
Gastric ulcers are one of the most prevalent types of peptic ulcer commonly seen in humans, affecting more than 10% of the global population [1]. The principal etiological factors associated with gastric ulcers are alcohol and non-steroidal anti-inflammatory drugs (NSAIDs) abuse, stress, smoking, and infection of H. pylori [2,3,4,5]. Alcohol consumption can directly interfere with gastric motility and metabolism. This action leads to mucosal damage and ulceration in the stomach [6]. Increasing evidence shows that an ethanol-induced gastric ulcer is closely associated with the generation of reactive oxygen species (ROS). Overproduction of ROS under oxidative stress results in cellular damage in the stomach. Gastric cells exhibit induction of several endogenous antioxidant enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) to maintain gastrointestinal homeostasis through the scavenging of ROS [7].
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