Moon Ji-Hyun, Choi Ah La, Noh Hyeon-Jeong, Song Jae Hwang, Hong Geum-Lan, Lee Nam Seob, Jeong Young-Gil, Han Seung Yun
Department of Anatomy, College of Medicine, Konyang University, Daejeon, Korea.
Department of Orthopedic Surgery, Konyang University Hospital, Daejeon, Korea.
Anat Cell Biol. 2024 Dec 31;57(4):559-569. doi: 10.5115/acb.24.117. Epub 2024 Aug 21.
Platelet-rich plasma (PRP) is a promising biomaterial rich in bioactive growth factors, offering potential as a therapeutic agent for various diseases. However, its effectiveness in central nervous system disorders like vascular dementia (VaD) remains underexplored. This study investigated the potential of PRP to mitigate VaD progression . A rat model of VaD was established via bilateral common carotid artery occlusion and hypovolemia operation. Rats were randomly assigned to receive either PRP or platelet-poor plasma (PPP)-the latter being a byproduct of PRP preparation and used as a reference standard-resulting in the groups designated as 'operated group (OP)+PRP' and 'OP+PPP', respectively. PRP or PPP (500 μl) was administered intraperitoneally on the day of the operation and postoperative days 2, 4, 6, and 8. Cognitive function was assessed using the Y-maze, Barnes maze, and passive avoidance tests. On postoperative day 8, hippocampal samples were subjected to histological and semi-quantitative analyses. OP exhibited significant memory decline compared to controls, while the 'OP+PRP' group showed notable improvement. Histological analysis revealed increased neuronal loss and neuroinflammation in OP hippocampi, mitigated in 'OP+PRP'. Semi-quantitative analysis showed decreased expression of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase B (TrkB) in OP, restored in 'OP+PPP' and further in 'OP+PRP'. These results highlight PRP's protective effects against VaD-induced hippocampal damage and cognitive impairment, partially attributed to BDNF/TrkB pathway upregulation.
富血小板血浆(PRP)是一种富含生物活性生长因子的有前景的生物材料,具有作为多种疾病治疗剂的潜力。然而,其在血管性痴呆(VaD)等中枢神经系统疾病中的有效性仍未得到充分探索。本研究调查了PRP减轻VaD进展的潜力。通过双侧颈总动脉闭塞和低血容量手术建立了VaD大鼠模型。将大鼠随机分为接受PRP或贫血小板血浆(PPP)——后者是PRP制备的副产品,用作参考标准——分别形成“手术组(OP)+PRP”组和“OP+PPP”组。在手术当天以及术后第2、4、6和8天腹腔注射PRP或PPP(500μl)。使用Y迷宫、巴恩斯迷宫和被动回避试验评估认知功能。在术后第8天,对海马样本进行组织学和半定量分析。与对照组相比,OP表现出明显的记忆衰退,而“OP+PRP”组显示出显著改善。组织学分析显示,OP海马体中神经元损失和神经炎症增加,而在“OP+PRP”组中减轻。半定量分析显示,OP中脑源性神经营养因子(BDNF)及其受体原肌球蛋白受体激酶B(TrkB)的表达降低,在“OP+PPP”组中恢复,在“OP+PRP”组中进一步恢复。这些结果突出了PRP对VaD诱导的海马损伤和认知障碍的保护作用,部分归因于BDNF/TrkB通路的上调。