Gallic acid (3,4,5-trihydroxybenzoic
acid, GA) is a phenolic compound found in many medicinal plants traditionally used in China or
patent medicine such as Feiyangchangweiyan
capsule (FY
capsule) for the treatment of
gastrointestinal diseases for decades. However, the evidence for the gastroprotective effect of GA is deficient and the pharmacological mechanisms remain limited. The present investigation was initiated to demonstrate the gastroprotective effect and to understand potential underlying mechanism of GA on
ethanol-induced
gastric ulcer in rats.
Gastric ulcers were induced by absolute
ethanol (5 mL/kg, i.g.) in male Sprague-Dawley rats, GA (10, 30, and 50 mg/kg), FY
capsule (0.4 g/kg) and 30 mg/kg
Lansoprazole was administered orally. Physiological saline and
lansoprazole were used as negative and positive control, respectively. Induction of rats with
ethanol resulted in a significant rise in
ulcer index, serum levels of inflammatory
cytokines markers (IL-1β, IL-6 and TNF-α),
TBARS,
protein expression of Bax and
Caspase-3 and a significant reduction in the activities or levels of
endogenous antioxidants (SOD, CAT and GSH), gastric mucosal protective factors (
PGE2 and NO) and
protein expression of Bcl-2. Pretreatment with GA showed a remarkable decrease in
ulcer index, inflammatory
cytokines markers,
TBARS,
protein expression of Bax and
Caspase-3 and a significant increase in the activities of
endogenous antioxidants, levels of
PGE2 and NO, and
protein expression of Bcl-2, Nrf2 and HO-1 when compared with
ethanol treated groups. This study demonstrated the gastroprotective effect of
Gallic acid and FY
capsule on
ethanol-induced
gastric ulcer in rats. The underlying mechanism of GA and FY
capsule against
gastric ulcer in rats caused by
ethanol might be involved in Nrf2/HO-1 anti-oxidative pathway and ultimately played an anti-apoptotic role through regulating Bax, Bcl-2 and
Caspase-3.