Rifaximin ameliorates depression-like behaviour in chronic unpredictable mild stress rats by regulating intestinal microbiota and hippocampal tryptophan metabolism

Feb 26, 2023Journal of affective disorders

Rifaximin reduces depression-like behavior in stressed rats by changing gut bacteria and brain tryptophan processing

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Abstract

Rifaximin administration improved depressive behaviour in rats subjected to chronic unpredictable mild stress.

Chronic unpredictable mild stress can induce depressive behaviours and alter gut microbiome composition.
Modulating gut microbiota may improve depression-like behaviour through the neuroendocrine pathway.
Tryptophan (TRP) metabolism is linked to depression, with its metabolites 5-hydroxytryptamine (5-HT) and kynurenine (KYN) involved in this process.
Rifaximin corrected intestinal microbiota disorders and regulated TRP metabolism in the hippocampus.
The treatment influenced the expression of key enzymes IDO1 and TPH2 associated with TRP metabolism.

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BACKGROUND: Chronic unpredictable mild stress (CUMS) can induce depressive behaviours and alter the composition of the gut microbiome. Although modulating gut microbiota can improve depression-like behaviour in rats, the mechanism of action is unclear. Additionally, gut microbiota can affect brain function through the neuroendocrine pathway. This pathway may function by regulating the secretion of neurotransmitters such as tryptophan (TRP). Metabolites of TRP, such as 5-hydroxytryptamine (5-HT) and kynurenine (KYN), are related to the pathophysiological process of depression. Indoleamine-2, 3-dioxygenase-1 (IDO1) and Tryptophan hydroxylase 2 (TPH2) are the key rate-limiting enzymes in TRP metabolism and play an important role in KYN and 5-HT metabolism.

METHODS: Rats were subjected to four weeks of CUMS and given rifaximin150 mg/kg by oral gavage daily. After modelling, we investigated the rat's behaviours, composition of the faecal microbiome, neurotransmitter metabolism and key metabolic enzymes of the TRP pathway in the hippocampus (HIP).

RESULTS: Rifaximin administration improved depressive behaviour in rats, corrected intestinal microbiota disorders and HIP TRP metabolism and regulated the expression of IDO1 and TPH2 in the HIP.

CONCLUSIONS: Rifaximin improves depression-like behaviour in CUMS rats by influencing the gut microbiota and tryptophan metabolism.

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Rifaximin ameliorates depression-like behaviour in chronic unpredictable mild stress rats by regulating intestinal microbiota and hippocampal tryptophan metabolism

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