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CNS Neurosci Ther ; 29(1): 471-482, 2023 01.
Artículo en Inglés | MEDLINE | ID: mdl-36419341

RESUMEN

PURPOSE: This study was to explore whether Ginkgo biloba extract (GBE) improve memory impairment by alleviating neuroinflammation signaling in mice with status epilepticus. METHODS: The status epilepticus (SE) mice model was established by pilocarpine and treated with 100 mg / kg of GBE for 14 days. Spontaneous alternation of Y-maze and new object recognition were used to explore memory impairment. To examine glial cell activation, we performed immunohistochemistry and immunofluorescence staining. The activation of NF-κB signaling and the expression level of lncRNA-COX2 were detected by Western blot and qRT-PCR, respectively. Adeno-associated virus lncRNA-COX2 was injected into mice for overexpression of lncRNA-COX2. RESULTS: After GBE treatment, the spontaneous alternation rate and the recognition coefficient in SE mice were both increased. Moreover, activation of glial cells, NF-κB signaling and lncRNA-COX2 were significantly decreased in SE mice. In the GBE-treated SE mice with lncRNA-COX2 overexpression, NF-κB signaling was up-regulated again; the reduced level of inflammation factors was reversed; the GBE-rescued spontaneous alternation rate of Y-maze was eliminated. CONCLUSION: Our results suggested that GBE reduces the hippocampal inflammation by down-regulating lncRNA-COX2 / NF-κB signaling in the SE mice, leading to the decrease of neuronal damage and the improvement of memory functions.


Asunto(s)
ARN Largo no Codificante , Estado Epiléptico , Ratones , Animales , FN-kappa B/metabolismo , ARN Largo no Codificante/genética , Ciclooxigenasa 2 , Extractos Vegetales/farmacología , Extractos Vegetales/uso terapéutico , Inflamación/tratamiento farmacológico , Inflamación/metabolismo , Trastornos de la Memoria/tratamiento farmacológico , Trastornos de la Memoria/etiología , Estado Epiléptico/inducido químicamente , Estado Epiléptico/tratamiento farmacológico
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