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DOI 10.4103/abr.abr_606_24

Медицинская библиотека · Advanced biomedical research · 2025

Pramipexole Exerts Beneficial Effects in a Rat Model of Acetic Acid-Induced Colitis via Modulating Inflammation.

Motavallian Azadeh, Ghazizadeh Foad, Khoshbin Sareh Pastaki, Karimian Paridokht, Aghajani Torshkooh Forough

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Аннотация

BACKGROUND

Inflammatory bowel disease (IBD) is a serious public health problem worldwide. The existing therapy options for IBD are limited and can cause severe difficulties, and thus require more research on alternative therapeutic techniques. Pramipexole is a dopamine receptor agonist with anti-inflammatory effects that was recently discovered. Given the importance of dopaminergic pathways in ulcerative colitis inflammation, we tested pramipexole's efficacy in a rat colitis model in this study.

MATERIALS AND

METHODS

Colitis was induced by administering 3% acetic acid intrarectally. Rats were randomly assigned to one of six groups: normal, colitis control, dexamethasone (1 mg/kg; i.p.), and pramipexole (0.25, 0.5, and 1 mg/kg; i.p.). In intestinal samples, macroscopic and microscopic lesion ratings, pro-inflammatory cytokine levels (tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta), and myeloperoxidase (MPO) activity were evaluated.

RESULTS

Compared to the colitis control group, pramipexole (0.5 and 1 mg/kg) substantially reduced macroscopic and microscopic intestinal damage, pro-inflammatory cytokine levels, and MPO activity. Furthermore, the indices mentioned above were considerably lower in the dexamethasone treatment group compared to the colitis control group.

CONCLUSIONS

Our findings indicate that pramipexole has favorable benefits in treating experimental colitis; however, further research is required to determine its clinical value as an IBD therapeutic agent.

Для цитирования: Motavallian Azadeh, Ghazizadeh Foad, Khoshbin Sareh Pastaki, Karimian Paridokht, Aghajani Torshkooh Forough. Pramipexole Exerts Beneficial Effects in a Rat Model of Acetic Acid-Induced Colitis via Modulating Inflammation.. Advanced biomedical research. 2025. DOI: 10.4103/abr.abr_606_24.
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