Aim: To investigate the protective effects of berberine on ethanol-induced gastric ulcer in mice. Methods: Gastric ulcers were induced by oral ingestion of ethanol. Nitric oxide (NO) content was measured, and mRNA expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Results: The ulcer index (UI) at 1 h, 2 h, 3 h and 6 h after oral administration of ethanol was 23.8■1.4,23.3■2.2,22.3■1.2 and 20.8■1.1, respectively. The UI in the berberine-treated groups (5 mg/kg and 50 mg/kg) was less than the control group. The content of NO in the control group was 73.3+7.3 μL/L, 94.0■9.2 μL/L, 109.6■ 6.4 μL/L and 138.2■10.2 μU/L in gastric juice and 5.8■1.1 μmol/g protein, 8.3■ 1.1 μmol/g protein, 9.8■ 1.1 μmol/g protein and 11.9■ 1.2 μmol/g protein in gastric tissue at 1 h, 2 h, 3 h and 6 h, respectively, after the oral administration of ethanol. The content of NO in the berberine-treated groups (5 mg/kg and 50 mg/kg) was higher than the control group at 1 h after the oral administration of ethanol (P<0.05), and was lower at 6 h (P<0.05). Analysis by RT-PCR showed that expression of eNOS was inhibited but iNOS expression was enhanced by ethanol. However, the expression of eNOS could be enhanced and iNOS expression could be inhibited by berberine (P<0.01). Conclusion: Berberine could significantly protect gastric mucosa from damage by ethanol. This effect may be related to the increased expression of eNOS mRNA and inhibited expression of iNOS mRNA. Aim: To investigate the protective effects of berberine on ethanol-induced gastric ulcer in mice. Methods: Gastric ulcers were induced by oral ingestion of ethanol. Nitric oxide (NO) content was measured, and mRNA expression of endothelial nitric oxide synthase (eNOS) Results of The ulcer index (UI) at 1 h, 2 h, 3 h and 6 h after oral administration of ethanol was 23.8. ■1.4,23.3■2.2, 22.3 ■1.2 and 20.8 ■1.1, respectively. The UI in the berberine-treated groups (5 mg/kg and 50 mg/kg) was less than the control group. The content of NO in the control The group was 73.3 + 7.3 μL/L, 94.0 ■ 9.2 μL/L, 109.6 ■ 6.4 μL/L and 138.2 ■10.2 μU/L in gastric juice and 5.8 ■ 1.1 μmol/g protein, 8.3 ■ 1.1 μmol/g protein, 9.8 ■ 1.1 μmol/g protein and 11.9 ■ 1.2 μmol/g protein in gastric tissue at 1 h, 2 h, 3 h and 6 h, respectively, after the oral administration of ethanol. The c Ontent of NO in the berberine-treated groups (5 mg/kg and 50 mg/kg) was higher than the control group at 1 h after the oral administration of ethanol (P<0.05), and was lower at 6 h (P< 0.05). Analysis by RT-PCR showed expression of eNOS was inhibited but iNOS expression was enhanced by ethanol. However, the expression of eNOS could be enhanced and iNOS expression could be inhibited by berberine (P<0.01). Concluded: Berberine could Significantly protect gastric mucosa from damage by ethanol. This effect may be related to the increased expression of eNOS mRNA and inhibited expression of iNOS mRNA.