Taurine modulates gut microbiota and attenuates inflammation in a rotenone-induced mouse model of Parkinson's disease.

Abstract

Parkinson's disease (PD) is a prevalent neurodegenerative disorder in which gut microbiota play a critical role in pathogenesis through the gut-brain axis. Taurine has been reported to exhibit neuroprotective properties. In this study, we employed a rotenone-induced mouse model of PD to investigate the protective effects of taurine and elucidate its underlying mechanisms. PD model mice exhibited weight loss and impaired motor function, both of which were significantly ameliorated by taurine treatment. These mice also showed a marked reduction in dopaminergic neurons alongside increased microglial and astrocyte activation in the substantia nigra. Taurine preserved dopaminergic neuron numbers and suppressed glial activation. Elevated plasma levels of LPS, IL-1β, IL-6, and TNF-α were detected in the PD model group, accompanied by intestinal barrier dysfunction, blood-brain barrier disruption, and gastrointestinal impairment. Taurine administration significantly reduced pro-inflammatory cytokine levels, improved gastrointestinal motility, and preserved the integrity of both the intestinal and blood-brain barriers. Fecal microbiota analysis revealed significant compositional alterations in PD mice. Both α- and β-diversity analyses indicated profound microbial dysbiosis in the model group, which was effectively mitigated by taurine.