BMC neuroscienceOct 8, 2026

Oral sodium butyrate reduces movement problems and loss of dopamine neurons in a rat model of Parkinson's disease

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Oct 9, 2026

Abstract

Sodium butyrate (NaB) may have therapeutic effects in models of Parkinson's disease (PD).

Short-chain fatty acids are involved in maintaining gut health and may influence the gut-brain connection.
The potential benefits of NaB for PD treatment are currently not well defined.
Animal models of PD, specifically those induced by 6-hydroxydopamine, may help clarify NaB's effects.
Evaluating NaB's impact in these models could support the development of new treatment strategies for PD.

Simplified

Short-chain fatty acids regulate intestinal homeostasis and modulate the gut-brain axis, suggesting they may be applicable in adjunctive treatments for Parkinson's disease (PD). However, the therapeutic efficacy of sodium butyrate (NaB) in PD remains unclear. Using appropriate PD animal models may aid in clarifying the therapeutic effects of NaB and facilitate the development of NaB-based PD treatment strategies. We comprehensively evaluated the therapeutic effects of oral NaB in rats with 6-hydroxydopamine (6-OHDA)-induced PD.

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Oral sodium butyrate reduces movement problems and loss of dopamine neurons in a rat model of Parkinson's disease

Abstract

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