In a 6-OHDA rat model of Parkinson's disease, oral rutin (10 mg/kg for 14 days) reduced intestinal inflammation—decreasing intraepithelial lymphocytes, goblet cell changes, and ileal Paneth cell hyperplasia—while selected gut bacterial taxa measured by PCR were unchanged.

This supports the idea that a dietary flavonoid can attenuate PD-related enteric inflammation and thus could be a candidate for gut-targeted adjunctive therapies influencing the gut-brain axis, though the study lacks central neuroprotection, behavioral outcomes, mechanistic depth, and comprehensive…

The enteric nervous system (ENS), a complex network of neurons and glial cells, is essential for maintaining intestinal homeostasis and is implicated in neurodegenerative diseases such as Parkinson's disease (PD). The gut-brain axis, modulated by gut microbiota (GM), is influenced by dietary compounds that can alter its composition. Despite advances in the understanding of PD pathophysiology, effective treatments remain limited, underscoring the need for novel therapeutic approaches. Among plant-derived compounds, the flavonoid rutin has shown significant antioxidant, anti-inflammatory, and neuroprotective properties in vivo. This study evaluated the effects of rutin on leukocyte infiltration, intestinal morphology, and GM composition in an experimental model of PD. Adult male Wistar rats received a stereotaxic injection of 6-hydroxydopamine (6-OHDA) and were treated orally with rutin (10 mg/kg) for 14 days. Intestinal segments were analyzed histomorphometrically, and fecal samples were assessed for the abundance of Firmicutes, Bacteroidetes, Prevotellacea, Entererobactereacea, Bifidobacterium sp and Lactobacillus sp. by PCR. Rutin administration significantly reduced intraepithelial lymphocyte infiltration and goblet cell numbers in the ileum and colon and prevented hyperplasia of Paneth cells in the ileum. Importantly, GM composition remained unchanged following rutin treatment. These findings demonstrated that rutin reduces intestinal inflammation in PD models without altering gut microbiota composition, highlighting its potential as a therapeutic strategy.