Adenosine A1 Receptor Agonist Protects Against Hippocampal Neuronal Injury After Lithium Chloride-Pilocarpine- Induced Epilepsy



Título del documento: Adenosine A1 Receptor Agonist Protects Against Hippocampal Neuronal Injury After Lithium Chloride-Pilocarpine- Induced Epilepsy
Revista: Revista de investigación clínica
Base de datos: PERIÓDICA
Número de sistema: 000454200
ISSN: 0034-8376
Autores: 1
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Instituciones: 1The Affiliated Hospital of Xuzhou Medical University, Epilepsy Center, Xuzhou, Jiangsu. China
Año:
Periodo: Mar-Abr
Volumen: 71
Número: 2
Paginación: 116-123
País: México
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Experimental, aplicado
Resumen en inglés Adenosine A1 receptor (AA1R) is widely present in the central nervous system, exerting brain protective antiepileptic effects, mainly by binding corresponding G proteins. We evaluated the neuroprotective effects of AA1R on hippocampal neuronal injury after lithium chloride-pilocarpine-induced epilepsy in rats. Materials and Methods A total of 60 male SD rats were randomly divided into four groups (n = 15/group): normal control, epilepsy, epilepsy + AA1R antagonist (DPCPX), and epilepsy + AA1R agonist (2-CAdo). An epilepsy model was established through kindling by lithium chloride-pilocarpine. The four groups were observed on days 1, 14, and 30. Pathological and morphological changes of hippocampal neurons were observed by HE staining; apoptosis was detected by TUNEL assay. Caspase-3 and GABA receptor expressions were detected by Western blot. Results In the hippocampal CA3 area of the epilepsy group, the cellular structure was not neatly arranged, and some neurons were swelling, thick, and incomplete. Compared with the epilepsy group at the same time point, cells in the epilepsy + DPCPX group had an increased distortion, disorganization, edema, cytoplasmic vacuoles, and degeneration. In the epilepsy + 2-CAdo group, cell arrangement was regular and orderly, and structural damages were lessened. Compared with the normal control group at the same time point, the epilepsy group underwent evident neuronal apoptosis, with a significantly higher apoptotic index (AI) (p < 0.05). Compared with the epilepsy group, the neuronal apoptosis of the epilepsy + DPCPX group was boosted, and the AI significantly increased (p < 0.05). The neuronal apoptosis of the epilepsy + 2-CAdo group was inhibited, and the AI significantly decreased (p < 0.05). Compared with the epilepsy group, the caspase-3 expression levels of the epilepsy + DPCPX group on days 14 and 30 were significantly upregulated (p < 0.05), but those of the epilepsy + 2-CAdo group were significantly
Disciplinas: Medicina
Palabras clave: Neurología,
Epilepsia,
Hipocampo,
Neuroprotectores,
Adenosina,
Receptores químicos
Keyword: Neurology,
Epilepsy,
Hippocampus,
Neuroprotectors,
Chemical receptors,
Adenosine
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