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Metformin alleviates reactive gliosis and neurodegeneration, improving cognitive deficit in a rat model of temporal lobe epilepsy.
Bojja, Sree Lalitha; Anand, Shashi; Minz, Ranjana W; Medhi, Bikash.
Afiliación
  • Bojja SL; Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka 576104, India.
  • Anand S; Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India.
  • Minz RW; Department of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India.
  • Medhi B; Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India. Electronic address: drbikashus@yahoo.com.
Brain Res ; 1844: 149138, 2024 Dec 01.
Article en En | MEDLINE | ID: mdl-39134259
ABSTRACT
Cognitive impairment is a prevalent co-morbidity associated with epilepsy. Emerging studies indicate that neuroinflammation could be a possible link between epilepsy and its comorbidities, including cognitive impairment. In this context, the roles of glial activation, proinflammatory mediators, and neuronal death have been well studied and correlated with epilepsy-associated cognitive impairment in animal studies. While recent reports have demonstrated the anti-epileptogenic and anti-convulsant actions of metformin, its effect on epilepsy associated cognitive deficit remains unknown. Therefore, the current study investigated the effect of metformin treatment on neuroinflammation, neurodegeneration, and cognitive deficits after inducing status epilepticus (SE) with lithium-pilocarpine in rats. Metformin treatment improved the hippocampal-dependent spatial and recognition memory in Morris water maze and Novel object recognition tasks, respectively. Further, metformin treatment attenuated microglial and astroglial activation, accompanied by reduced IL-1ß, COX-2 and NF-Ä¸ß gene expression. Additionally, metformin conferred neuroprotection by inhibiting the neuronal death as assessed by Nissl staining and transmission electron microscopy. These findings suggest that metformin holds promise as a therapeutic intervention for cognitive impairment associated with epilepsy, possibly through its modulation of glial activation and neuronal survival. Further research is needed to elucidate the precise mechanisms and to assess the long-term effect of metformin in epilepsy-associated cognitive impairment.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Modelos Animales de Enfermedad / Epilepsia del Lóbulo Temporal / Disfunción Cognitiva / Gliosis / Metformina Límite: Animals Idioma: En Revista: Brain Res Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Modelos Animales de Enfermedad / Epilepsia del Lóbulo Temporal / Disfunción Cognitiva / Gliosis / Metformina Límite: Animals Idioma: En Revista: Brain Res Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos