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Inflammatory bowel disease (IBD) comprises a spectrum of diseases characterized by chronic inflammation of the gastrointestinal tract without a specific cause or pathogen. Gabapentin (GBP) is an anticonvulsant drug, but previous studies show that it is effective in reducing gastric inflammatory damage and decreasing the acute inflammatory process. During colitis, there is an increase in substances that act on the endocannabinoid pathway, which are important for protecting the colon during the development of the inflammatory intestinal process. Therefore, the aim of this study was to analyze the anti-inflammatory effect of GBP on acetic acid (AA)-induced colitis in mice and to see whether this mechanism of action is due to the pharmacological endocannabinoid pathway. The results show that AA was effective in inducing ulcerative colitis (UC); that GBP reduces inflammation in the colon caused by AA, however, its effect is probably independent of the endocannabinoid receptor pathway,which is not involved in reducing the inflammatory effect of experimentally induced UC, showing that this pathway does not represent a promising therapeutic alternative for patients with UC.