Abstract
Polygonum cuspidatum is widely used as food and medicine in Korea, China, and Japan. Its major bioactive components, resveratrol and emodin, reportedly protect against gastric lesions. We therefore aimed to investigate: (1) the gastroprotective effects of P. cuspidatum roots in hydrochloric acid/ethanol (HCl/EtOH)- and indomethacin-induced acute gastric ulcer rat models; (2) the healing effects in an acetic acid-induced ulcer model; and (3) potential mechanisms by measuring gastric acid secretion-related parameters in a pyloric ligation-induced ulcer model, and by measuring antioxidant enzyme and prostaglandin E2 levels in the gastric tissue of HCl/EtOH-treated rats. Oral administration of P. cuspidatum extract (PCE) at doses of 100 and 300 mg/kg significantly decreased HCl/EtOH- and indomethacin-induced gastric lesions. PCE at 300 mg/kg significantly reduced gastric lesions in acetic acid-induced ulcers. PCE increased superoxide dismutase (SOD) activity and glutathione (GSH) and prostaglandin E2 levels in gastric tissue, whereas it did not alter gastric acid secretion-related parameters. Our findings indicate that PCE has gastroprotective effects against HCl/EtOH and non-steroidal anti-inflammatory drugs (NSAIDs) and promotes healing of acetic acid-induced ulcers. These gastric mucosal protection and ulcer healing effects are associated with antioxidant effects and the augmentation of prostaglandin E2 and suggest that P. cuspidatum might be a promising preventive and therapeutic agent for treating gastric ulcers.
Highlights
Gastric ulcers result from damage to the mucosal lining of the stomach due to an increase in aggressive factors such as reactive oxygen species (ROS) and gastric acid, and a decrease in protective factors such as prostaglandins and mucus [1,2]
We first demonstrated that P. cuspidatum extract (PCE) pretreatment prevents acute gastric mucosal injury induced by both HCl/EtOH and indomethacin, while PCE post-treatment promotes the healing of acetic acid-induced chronic gastric lesions
Our study shows that seven days of PCE treatment after ulcer induction with acetic acid reduced gastric lesions, whereas a comparable treatment regimen with omeprazole did not
Summary
Gastric ulcers result from damage to the mucosal lining of the stomach due to an increase in aggressive factors such as reactive oxygen species (ROS) and gastric acid, and a decrease in protective factors such as prostaglandins and mucus [1,2]. The most common symptom is upper abdominal pain, which occurs at night and is relieved by food intake [3]. Gastric ulcers are very painful and lower the quality of life of those who suffer from them [4]. Lack of proper gastric ulcer treatment can induce gastrointestinal bleeding, perforation, and gastric outlet obstruction [5]. In South Korea, about 10% of people have suffered from gastric ulcers [6]. Lifestyle habits, such as excessive alcohol intake or prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs), are factors that cause gastritis and gastric ulcer [7]. Infection by the common bacteria Helicobacter pylori is another significant cause of gastric ulcers
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