The present study investigated
benexate hydrochloride
betadex (BHB)-mediated
ulcer healing, and changes to microcirculation modulated through
nitric oxide synthase (NOS) and anti-inflammatory activity. A rat model of gastric mucosal injury was established through injection of a 60%
acetic acid solution into the stomach. Following
ulcer induction, the rats were administered BHB orally for 5 days at doses of 0, 100, 300 or 1,000 mg/kg. The highest dose of BHB was also administered with or without L-
NG-nitroarginine methyl ester (
L-NAME). The area of
gastric ulcers was determined by planimetry, and expression of
cyclooxygenases (COX),
cytokines and NOS in stomach tissues were measured using western blotting. Compared with the control group,
gastric ulcer size was significantly decreased in the 1,000 mg/kg BHB-treated group (P<0.05). Administration of BHB led to a significant increase in endothelial (e)NOS expression (P<0.05). Although
acetic acid co-treatment with
L-NAME induced more severe mucosal damage, BHB decreased COX expression and
tumor necrosis factor-α levels when administered with the
nitric oxide inhibitor,
L-NAME (P<0.05). BHB exhibited protective effects in a rat model of
gastric ulcers, which were associated with a decrease in pro-inflammatory
cytokine levels and the activation of eNOS.