Propylparaben Reduces the Long-Term Consequences in Hippocampus Induced by Traumatic Brain Injury in Rats: Its Implications as Therapeutic Strategy to Prevent Neurodegenerative Diseases
Issue title: Translational Research and Drug Discovery for Neurodegeneration: Challenges for Latin America
Guest editors: K.S. Jagannatha Rao, Gabrielle B. Britton, Luisa Lilia Rocha Arrieta, Norberto Garcia-Cairasco, Alberto Lazarowski, Adrián Palacios, Antoni Camins Espuny and Ricardo B. Maccioni
Affiliations: [a] Department of Pharmacobiology, Center for Research and Advanced Studies (CINVESTAV), Mexico City, Mexico
| [b] Institute of Neurobiology, National Autonomous University of Mexico, Campus Juriquilla, Queretaro, Mexico
| [c] Unit for Medical Research in Neurological Diseases, Specialties Hospital, National Medical Center SXXI (CMN-SXXI), Mexico City, Mexico
Correspondence:
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Correspondence to: Dr. Luisa Rocha, Pharmacobiology Department, Center for Research and Advanced Studies, Calz. Tenorios 235. Col. Granjas Coapa, Mexico City 14330, Mexico. Tel.: +52 55 54 83 28 59; E-mail: lrocha@cinvestav.mx.
Abstract: Background:Severe traumatic brain injury (TBI), an important risk factor for Alzheimer’s disease, induces long-term hippocampal damage and hyperexcitability. On the other hand, studies support that propylparaben (PPB) induces hippocampal neuroprotection in neurodegenerative diseases. Objective:Experiments were designed to evaluate the effects of subchronic treatment with PPB on TBI-induced changes in the hippocampus of rats. Methods:Severe TBI was induced using the lateral fluid percussion model. Subsequently, rats received subchronic administration with PPB (178 mg/kg, TBI+PPB) or vehicle (TBI+PEG) daily for 5 days. The following changes were examined during the experimental procedure: sensorimotor dysfunction, changes in hippocampal excitability, as well as neuronal damage and volume. Results:TBI+PEG group showed sensorimotor dysfunction (p < 0.001), hyperexcitability (64.2%, p < 0.001), and low neuronal preservation ipsi- and contralateral to the trauma. Magnetic resonance imaging (MRI) analysis revealed lower volume (17.2%; p < 0.01) and great damage to the ipsilateral hippocampus. TBI+PPB group showed sensorimotor dysfunction that was partially reversed 30 days after trauma. This group showed hippocampal excitability and neuronal preservation similar to the control group. However, MRI analysis revealed lower hippocampal volume (p < 0.05) when compared with the control group. Conclusion:The present study confirms that post-TBI subchronic administration with PPB reduces the long-term consequences of trauma in the hippocampus. Implications of PPB as a neuroprotective strategy to prevent the development of Alzheimer’s disease as consequence of TBI are discussed.
