Bupropion Ameliorates Acetic Acid–Induced Colitis in Rat: the Involvement of the TLR4/NF-kB Signaling Pathway

Rashidian, Amir and Dejban, Pegah and Karami Fard, Kiana and Abdollahi, Alireza and Hasanvand, Amin (2020) Bupropion Ameliorates Acetic Acid–Induced Colitis in Rat: the Involvement of the TLR4/NF-kB Signaling Pathway. Inflammation.

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Abstract

Abstract—InflammatoryboweldiseasecomposedofulcerativecolitisandCrohn’sdiseaseisa disorder that may involve entire gastrointestinal tract. Its pathogenesis is mainly an immunemediated inflammation. Recently, it has been indicated that bupropion possesses antiinflammatory properties; hence, the objective of this experiment is the investigation of the anti-inflammatory influence of bupropion on colonic lesions that emerged following the intrarectal administration of acetic acid. Thirty-six male Wistar rats were allocated randomly intosix groups, including control,acetic acid, dexamethasone (2 mg/kg), and bupropion (40, 80, and 160 mg/kg). Colitis was induced by intrarectal administration of acetic acid in all study groups except control group, and animals were treated by oral administration of dexamethasone and bupropion. While macroscopic and microscopic lesions were observed after colitis induction, administration of dexamethasone and bupropion 160 mg/kg led to the remarkable improvement in lesions. In addition, the expression of TLR4 and NF-ĸB was decreased after colitis induction; however, treatment with dexamethasone (2 mg/kg) and bupropion (160 mg/kg) resulted in a significant decrease in their expression. Regarding biochemical factors, following colitis induction, TNF-α level and MPO activity were increased; nevertheless, dexamethasone (2 mg/kg) and bupropion (160 mg/kg) decreased the TNF-α and MPO activity. In conclusion, bupropion exerts anti-inflammatory influence through suppressing the TLR4 and NF-ĸB expression in the rat model of acute colitis.

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