Open AccessEffects of platelet‐rich plasma on the memory impairment, apoptosis, and hippocampal synaptic plasticity in a rat model of hepatic encephalopathy
Author(s) -
Bayat Mahnaz,
Khalili Azadeh,
Bayat Gholamreza,
Akbari Somayeh,
Yousefi Nejad Amirhossein,
Borhani Haghighi Afshin,
Haghani Masoud
Publication year - 2022
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.2447
Subject(s) - synaptic plasticity , long term potentiation , morris water navigation task , hippocampus , neurotransmitter , neuroprotection , hippocampal formation , hepatic encephalopathy , neurotransmission , neuroscience , medicine , psychology , endocrinology , anesthesia , central nervous system , cirrhosis , receptor
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.