Anthraquinone Derivative Rufigallol Protects Against Ethanol-Induced Gastric Damage via Modulation of PGE₂, NO, and...

Excessive ethanol consumption is a cause of gastric ulceration. This study aimed to identify the gastroprotective action of rufigallol, an anthraquinone, against ethanol-induced gastric ulcers and assess its antioxidant and anti-inflammatory properties. Healthy rats were grouped into five groups (n = 8); the control group received sterile saline orally; the ethanol group received ethanol (5 mL/kg) to generate gastric ulcers on the last day of the experiment; the pretreated rufigallol group was administered 10 or 20 mg/kg rufigallol orally for a week before gastric ulcer initiation; and the drug control group received omeprazole (20 mg/kg) for a week with ethanol treatment. The results showed that oral rugalallol significantly reduced gastric ulcers, as indicated by decreased gastric juice volume and increased preventive percentage, gastric pH value, and pepsin activity. Histopathology confirmed a reduction in the gastric ulcer index following rufigallol treatment. Rufigallol pre-treatment significantly increased antioxidant levels (CAT, SOD, and GSH) and decreased MDA levels compared to the ethanol group. Furthermore, rufigallol treatment decreased MPO, pro-inflammatory cytokines, and mediator levels. It also reduced COX-2, IFN-γ, and NLRP3 expression and restored NO and PGE2 levels. In vitro experiments using HT-29 and HaCaT cell lines confirmed that rufigallol reduced cytokine production and exhibited anti-inflammatory activity in response to lipopolysaccharide stimulation. These results suggested that rufigallol administration may provide gastroprotective benefits against ethanol-induced gastric ulcers, potentially by reducing oxidative stress and gastric inflammation.