Leydianne Leite de Siqueira Patriota, Emanuel Davi Lima de Matos Leão, Maria Nívea Bezerra da Silva, Amanda de Oliveira Marinho, Bárbara Raíssa Ferreira de Lima, Jainaldo Alves da Costa, Luciclaudio Cassimiro de Amorim, Valéria Bianca de Souza Santos, Patrícia Maria Guedes Paiva, Michelly Cristiny Pereira, Daniella Carla Napoleão, Jorge Vinícius Fernandes Lima Cavalcanti, Leucio Duarte Vieira, Michelle Melgarejo da Rosa, Thiago Henrique Napoleão
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.