Supplementation of the Probiotic LLH135 Reduces Oxidative Stress in a Model of Hemiparkinsonism

Oxidative stress and neuroinflammation are considered as the two main etiological reasons behind idiopathic Parkinson's disease (PD). Nevertheless, the actual treatments are focused on improving motor symptoms by restoring dopamine (DA) presence, leaving said causes unattended. Probiotics could be a promising strategy for the improvement of these physiological features behind the disease and therefore constitute a complementary treatment for those having PD. This study evaluated the effect of the oral administration of a probiotic bacteria mixture from 3 strains of <i>Limosilactobacillus fermentum</i> LH01<i>, Limosilactobacillus reuteri</i> LH03, and <i>Lactiplantibacillus plantarum</i> LH05 (LLH135), of human milk origin, for 4 weeks, on mice under the hemiparkinsonism model of intrastriatal administration of 6-hidroxidopamine (6-OHDA). We measured total antioxidant capacity (TAC), super oxide dismutase (SOD) activity, and 8-deoxyguanosine (8-OHdG) regarding oxidative stress. Concerning neuroinflammation, immunoreactivity for GFAP, IBA-1, and CD68 was measured by immunohistochemistry and the latter markers corroborated in colocalization with immunofluorescence to assess activated microglia. The probiotic mixture diminished the oxidative stress features of SOD activity as well as 8-OHdG generated by the model of hemiparkinsonism. These effects were accompanied as well by the dampening of the glial immunoreactivity and colocalization of IBA-1 and CD68 that were present under the model. Our findings suggest that the administration of the probiotic LLH135 exerts neuroprotective effects by promoting an antioxidant response which could be explained by the modulation of the response from glial cells to dopaminergic neuronal damage induced with 6-OHDA.