Sailian Li¹ , Zengshu Xing², Bao Xu¹, Xiaoxi Huang¹, Jiankang Zhang², Mengyu Zhang²

Abstract

Purpose: To study the effect of evodiamine on the signaling pathway of ROS/ICAM-1/Nrf2 in rats with acetic acid-induced stomach ulcers. Methods: The rats were randomly assigned to five groups containing 10 rats each. Prior to acetic acid-induction of gastric ulcers, omeprazole (4.0 mg/kg/day), low-dose evodiamine (L-EVD, 20 mg/kg/day), and high-dose evodiamine (H-EVD, 40 mg/kg/day) were orally administered to the respective groups for 15 days. Following ulcer induction, the same treatments continued for an additional 7 days, for a total treatment duration of 22 days. The control (0.9 % saline) and acetic acid (model) groups were administered 0.9 % sodium chloride solution (10 mL/kg) for the same period. Thereafter, oxidative stress, inflammatory markers, macroscopic and microscopic evaluations were conducted on the gastric mucosa. Results: The acetic acid group showed significantly higher levels of oxidative and inflammatory markers, as well as damage and degeneration of the gastric mucosa when compared to control group (p < 0.05). However, both low-dose and high-dose evodiamine treatment groups demonstrated significant gastric healing. Administration of low-dose and high-dose evodiamine resulted in significantly lower levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO) and intracellular adhesion molecule-1 (ICAM-1, p < 0.05). Furthermore, evodiamine treatment led to significantly increased levels of glutathione (GSH) and nuclear fact-erythroid factor 2 (Nrf2). Conclusion: Evodiamine reduces oxidative stress, suppresses inflammatory reactions, and exerts an anti-ulcer effect on acetic acid-induced gastric ulcers in rats by modulating ROS/ICAM-1/Nrf2 signaling pathway. More studies into the integration of evodiamine into conventional pharmaceutical treatments for gastric ulcers should be conducted.