Coriander (Coriandrum sativum L. leaves) improves brain and gut pathology in mouse models of brain-first and gut-first Parkinson's disease.

Abstract

Recently, an increasing number of studies have focused on the microbiota-gut-brain axis in Parkinson's disease (PD), and a new perspective has emerged regarding the regulation of gut health and the microbiome as potential treatments for PD. We focused on coriander, which is consumed worldwide and exhibits significant anti-inflammatory and antimicrobial activities. In this study, we investigated whether coriander ameliorated PD phenotypes in both brain-first and gut-first PD models. C57BL/6J mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or Proteus mirabilis (P. mirabilis) for 5 d. In the MPTP-induced model, coriander (30 and 100 mg/kg), including the MPTP injection period, was administered orally for 15 d. In the P. mirabilis-induced model, coriander (100 mg/kg) was administered orally for 21 d, including the period of P. mirabilis administration. The results showed that coriander ameliorated MPTP- and P. mirabilis-induced motor deficits and dopaminergic neuronal death in mice, and suppressed inflammatory responses in both the brain and colon. In addition, coriander improved P. mirabilis-induced α-synuclein pathology in both brain and colon. Coriander reduced the mRNA expression of P. mirabilis and hemolysin A (HpmA) in feces, an endotoxin factor produced by P. mirabilis, in MPTP-induced and P. mirabilis-induced models. These results indicate that coriander has the potential to attenuate PD pathology in the brain and gut in both the brain-first and gut-first PD models. This suggests that coriander is a promising functional food for the prevention and treatment of PD.