Moringa oleifera Lam. Seed Lectin (WSMoL) Attenuates Parkinsonian Symptoms in Mice via Anti-Inflammatory, Antioxidant, and Neurotransmitter-Modulating Effects.

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This work investigated the effects of Moringa oleifera seed lectin (WSMoL) on motor performance, neuroinflammation, and oxidative stress in a rotenone-induced model of Parkinson's disease (PD). Male mice were daily administered rotenone (3 mg/kg, i.p.) 1 h after being treated with WSMoL (1, 2, or 4 mg/kg, i.p.), levodopa (L-DOPA, 10 mg/kg), or vehicle for 10 days. To assess dopaminergic involvement, another group received the D1 receptor antagonist SCH-23390 co-administered with WSMoL (4 mg/kg). The healthy control group received vehicle only. Motor performance was evaluated using the rotarod, cylinder, and open field tests. Brain levels of monoamines and cytokines as well as redox status were measured. WSMoL prevented the rotenone-related deficits in motor performance, which was accompanied by non-depleted dopamine and serotonin levels. WSMoL also mitigated the increase of IL-6, IL-17A, IFN-γ, and TNF-α. In addition, it prevented oxidative stress by avoiding the exacerbation of superoxide production, lipid peroxidation, and NADPH oxidase activity, while maintaining catalase, superoxide dismutase (SOD), and reduced glutathione (GSH) levels. The data show that D1 receptor-mediated signaling contributes to WSMoL effects. In conclusion, WSMoL attenuates motor deficits and neuroinflammation in a PD model, which supports its potential as a neuroprotective agent and warrants further mechanistic and translational studies.

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