Methotrexate (MTX) is widely used for treating cancers and inflammatory diseases; it is a potential anti-metabolite and folate antagonist. We investigated potential protective effects of benfotiamine on MTX damage. We used a rat model of MTX induced gastric injury to assess changes in gastric histopathology, oxidative stress and visfatin levels due to MTX treatment. Rats were divided into four groups: an untreated control group, an MTX group treated with a single dose of MTX, a benfotiamine group treated with benfotiamine daily for two weeks, and a benfotiamine + MTX group treated with a single dose of MTX followed by benfotiamine daily for two weeks. Total tissue antioxidant status (TAS), total oxidant status (TOS) and visfatin levels were measured at the end of the experiment. At the end of the experiment, we investigated both visfatin expression and the histopathology of gastric tissues. The mean visfatin level was lower in the MTX group than in the benfotiamine group. The mean tissue TOS levels were higher in MTX group than in the control, benfotiamine or benfotiamine + MTX groups. Significant gastric gland dilation, and erosion and loss of mucosa were found on the gastric surface in the MTX group compared to the control group. The dilation, erosion and mucosal loss were decreased significantly in the benfotiamine + MTX group compared to the MTX group. Compared to the control group, visfatin immunoreactivity was reduced significantly in the MTX group. Decreased visfatin levels appear to play a role in the mechanism of gastric damage. Benfotiamine may be useful for preventing MTX induced gastric injuries.
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