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

Mario E Flores-Soto1, Angelica Y Nápoles-Medina1,2, Aldo R Tejeda-Martínez1

  • 1Laboratorio de Neurobiología Celular y Molecular, División de Neurociencias, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social, Guadalajara, Jalisco, Mexico.

Behavioural Neurology
|April 21, 2025
PubMed

Insights

This study shows that a probiotic mixture (LLH135) reduced oxidative stress and neuroinflammation in a Parkinson

Area of Science:

  • Neuroscience
  • Microbiology
  • Pharmacology

Background:

  • Parkinson's disease (PD) is linked to oxidative stress and neuroinflammation, yet current treatments primarily address motor symptoms.
  • Existing therapies for Parkinson's disease do not target the underlying causes of oxidative stress and neuroinflammation.
  • Probiotics offer a potential complementary strategy for managing the physiological factors contributing to Parkinson's disease.

Purpose of the Study:

  • To investigate the neuroprotective effects of a specific probiotic mixture (LLH135) in a mouse model of Parkinson's disease.
  • To evaluate the impact of LLH135 on oxidative stress markers and neuroinflammation.
  • To determine if LLH135 can modulate glial cell responses to dopaminergic neuronal damage.

Main Methods:

  • Oral administration of a probiotic mixture (LLH135) containing three *Limosilactobacillus* and *Lactiplantibacillus* strains for 4 weeks.
  • Utilized a 6-hydroxydopamine (6-OHDA) induced hemiparkinsonism mouse model.
  • Assessed oxidative stress via total antioxidant capacity (TAC), superoxide dismutase (SOD) activity, and 8-deoxyguanosine (8-OHdG) levels.
  • Measured neuroinflammation using immunohistochemistry for GFAP, IBA-1, and CD68, and immunofluorescence for activated microglia colocalization.

Main Results:

  • The LLH135 probiotic mixture significantly reduced SOD activity and 8-OHdG levels, indicating diminished oxidative stress.
  • Probiotic administration dampened glial cell activation, evidenced by reduced GFAP, IBA-1, and CD68 immunoreactivity.
  • The study observed a decrease in activated microglia, confirmed by colocalization of IBA-1 and CD68 markers.

Conclusions:

  • Oral administration of the probiotic LLH135 demonstrates significant neuroprotective effects in a Parkinson's disease model.
  • LLH135 promotes an antioxidant response and modulates glial cell activity, mitigating dopaminergic neuronal damage.
  • This probiotic mixture represents a promising complementary therapeutic approach for Parkinson's disease by targeting oxidative stress and neuroinflammation.