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Effects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy

OBJECTIVES: In the present study, we aimed to determine whether intraperitoneal injection of platelet‐rich plasma (PRP) could have a neuroprotective effect on learning, memory, and synaptic plasticity impairment as well as hippocampal apoptosis in rats with hepatic encephalopathy induced by bile duc...

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Detalles Bibliográficos
Autores principales: Bayat, Mahnaz, Khalili, Azadeh, Bayat, Gholamreza, Akbari, Somayeh, Yousefi Nejad, Amirhossein, Borhani Haghighi, Afshin, Haghani, Masoud
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8785608/
https://www.ncbi.nlm.nih.gov/pubmed/34855284
http://dx.doi.org/10.1002/brb3.2447
Descripción
Sumario:OBJECTIVES: In the present study, we aimed to determine whether intraperitoneal injection of platelet‐rich plasma (PRP) could have a neuroprotective effect on learning, memory, and synaptic plasticity impairment as well as hippocampal apoptosis in rats with hepatic encephalopathy induced by bile duct ligated (BDL). METHODS: The rats were divided into four groups: the control, sham, BDL+ V (vehicle), and BDL+ PRP. The BDL rats were treated with PRP immediately after the surgery, and the injection was done every 3 days for 30 days. The passive avoidance and Morris water maze tests were used for the evaluation of learning and memory. The long‐term potentiation (LTP), basal‐synaptic transmission, and paired‐pulse ratio, as an index for measurement of neurotransmitter release probability, were evaluated by field‐potential recording. After taking a blood sample for assessment of the liver enzymes, the animals were sacrificed and their hippocampus was removed for evaluation of cleaved caspase‐3 by Western blot. RESULTS: Serological assessment of the liver function showed that BDL severely impaired the liver function. Also, PRP treatment could partially improve the liver dysfunction along with recovery in fear memory and spatial learning memory performance, LTP, basal‐synaptic transmission, and neurotransmitter release probability. PRP‐treated rats also showed a significant reduction in neuronal apoptosis in the CA1 area. CONCLUSIONS: The results of this study suggest that PRP improves cognitive performance and synaptic plasticity in BDL rats via direct neuroprotective property and/or indirectly by improvement of hepatic dysfunction.