Estudio de la ruta neurotrófica Pleiotrofina/PTPRZ en el hipocampo de ratas expuestas a consumo crónico de alcohol y/o deficiencia de tiamina

Autores/as

  • Laura Orio Universidad Complutense de Madrid
  • Rosario López-Rodríguez Universidad San Pablo-CEU
  • Marta Moya Universidad Complutense de Madrid
  • Esther Gramage Universidad San Pablo-CEU
  • Gonzalo Herradón Universidad San Pablo-CEU

Palabras clave:

Wernicke, Korsakoff, deficiencia de tiamina, pleiotrofina, receptor proteína tirosina Fosfatasa Z, neuroinflamación, hipocampo

Resumen

La encefalopatía de Wernicke (WE) es una enfermedad neurológica causada por la deficiencia de tiamina (TD) cuyo principal factor de riesgo es el trastorno por uso del alcohol. El objetivo de este estudio es explorar el perfil de expresión de genes candidatos relacionados con neuroinflamación, disfunción mitocondrial y metabolismo de la tiamina en el hipocampo de animales expuestos a consumo crónico de alcohol (CA), una dieta deficiente en tiamina (TDD) o la combinación de ambos. Se analizaron un total de 42 ratas Wistar macho incluidas en 4 grupos experimentales: control (C) que recibieron agua o agua suplementada con tiamina (0,2 g/L), alcohol crónico (CA) durante 36 semanas, dieta TD y piritiamina durante 12 días (TDD) y un grupo que combinaba CA+TDD. La expresión relativa de factores neurotróficos (Ptn, Mdk, Ptprz), factores proinflamatorios (Tlr4, Ccl2 y Hmgb1), proteínas implicadas en homeostasis mitocondrial (Mfn1 y Mfn2) y enzimas del metabolismo de la tiamina (Tpk1) se determinó a partir de ARNm obtenido del hipocampo de los distintos grupos experimentales. El análisis estadístico se realizó mediante el test no paramétrico Kruskal-Wallis. La expresión de Ptprz tendía a ser menor en el grupo TDD comparado con el grupo C (no significativo) mientras que la disminución de Ptprz observada en el grupo TDD fue estadísticamente significativa cuando se comparaba con el grupo CA+TDD (p<0,05). Además, el grupo TDD mostró los menores niveles de expresión de Ptn y esta disminución fue estadísticamente significativa comparada con los grupos C y CA (p<0,05). Nuestros resultados indican un perfil diferencial de expresión de la ruta PTN-MDK-PTPRZ en el hipocampo de ratas con una dieta TD distinto al observado en el resto de los modelos de encefalopatía WE analizados (CA y CA+TDD).

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2025-12-23

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