Flores-Soto Mario E, Nápoles-Medina Angelica Y, Tejeda-Martínez Aldo R, Solís-Pacheco Josué R, Chaparro-Huerta Verónica, Gutiérrez-Sevilla Juan E, Aguilar-Uscanga Blanca R
Laboratorio de Neurobiología Celular y Molecular, División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Mexico.
Laboratorio de Investigación Leche humana, Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Guadalajara, Jalisco, Mexico.
Behav Neurol. 2025 Apr 10;2025:8401392. doi: 10.1155/bn/8401392. eCollection 2025.
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 LH01 LH03, and 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.
氧化应激和神经炎症被认为是特发性帕金森病（PD）背后的两个主要病因。然而，目前的实际治疗方法主要集中在通过恢复多巴胺（DA）的水平来改善运动症状，而忽略了上述病因。益生菌可能是改善该疾病背后这些生理特征的一种有前景的策略，因此可作为帕金森病患者的辅助治疗方法。本研究评估了口服源自人乳的3种菌株LH01、LH03和LH05（LLH135）的益生菌混合物4周，对经纹状体内注射6-羟基多巴胺（6-OHDA）建立的偏侧帕金森病模型小鼠的影响。我们测量了与氧化应激相关的总抗氧化能力（TAC）、超氧化物歧化酶（SOD）活性和8-脱氧鸟苷（8-OHdG）。关于神经炎症，通过免疫组织化学测量了GFAP、IBA-1和CD68的免疫反应性，并通过免疫荧光对后一种标志物进行共定位，以评估活化的小胶质细胞。益生菌混合物减少了偏侧帕金森病模型产生的SOD活性以及8-OHdG等氧化应激特征。这些作用还伴随着模型中存在的胶质细胞免疫反应性的减弱以及IBA-1和CD68的共定位。我们的研究结果表明，给予益生菌LLH135可通过促进抗氧化反应发挥神经保护作用，这可能是由于调节了胶质细胞对6-OHDA诱导的多巴胺能神经元损伤的反应来解释的。
