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Therapeutic efficacy of cinnamein, a component of balsam of Tolu/Peru, in controlled cortical impact mouse model of TBI.
Poddar, Jit; Rangasamy, Suresh B; Pahan, Kalipada.
Afiliación
  • Poddar J; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, 60612, USA.
  • Rangasamy SB; Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, 60612, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, 60612, USA.
  • Pahan K; Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, 60612, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, 60612, USA. Electronic address: Kalipada_Pahan@rush.edu.
Neurochem Int ; 176: 105742, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38641028
ABSTRACT
Traumatic brain injury (TBI) remains a major health concern which causes long-term neurological disability particularly in war veterans, athletes and young adults. In spite of intense clinical and research investigations, there is no effective therapy to cease the pathogenesis of the disease. It is believed that axonal injury during TBI is potentiated by neuroinflammation and demyelination and/or failure to remyelination. This study highlights the use of naturally available cinnamein, also chemically known as benzyl cinnamate, in inhibiting neuroinflammation, promoting remyelination and combating the disease process of controlled cortical impact (CCI)-induced TBI in mice. Oral delivery of cinnamein through gavage brought down the activation of microglia and astrocytes to decrease the expression of inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) in hippocampus and cortex of TBI mice. Cinnamein treatment also stimulated remyelination in TBI mice as revealed by PLP and A2B5 double-labeling, luxol fast blue (LFB) staining and axonal double-labeling for neurofilament and MBP. Furthermore, oral cinnamein reduced the size of lesion cavity in the brain, improved locomotor functions and restored memory and learning in TBI mice. These results suggest a new neuroprotective property of cinnamein that may be valuable in the treatment of TBI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Modelos Animales de Enfermedad / Lesiones Traumáticas del Encéfalo Límite: Animals País/Región como asunto: America do sul / Peru Idioma: En Revista: Neurochem Int Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Modelos Animales de Enfermedad / Lesiones Traumáticas del Encéfalo Límite: Animals País/Región como asunto: America do sul / Peru Idioma: En Revista: Neurochem Int Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido