Platelet-rich plasma protects hippocampal neurons and memory functions in a rat model of vascular dementia.

IF 1.4 Q3 ANATOMY & MORPHOLOGY Anatomy & Cell Biology Pub Date : 2024-08-21 DOI:10.5115/acb.24.117
Ji-Hyun Moon, Ah La Choi, Hyeon-Jeong Noh, Jae Hwang Song, Geum-Lan Hong, Nam Seob Lee, Young-Gil Jeong, Seung Yun Han
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Abstract

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 in vivo. 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.

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富血小板血浆可保护血管性痴呆大鼠模型中的海马神经元和记忆功能。
富血小板血浆(PRP)是一种富含生物活性生长因子的生物材料,具有治疗各种疾病的潜力。然而,它对血管性痴呆(VaD)等中枢神经系统疾病的疗效仍未得到充分探索。本研究调查了 PRP 在体内缓解血管性痴呆进展的潜力。通过双侧颈总动脉闭塞和低血容量手术建立了大鼠血管性痴呆模型。大鼠被随机分配接受 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),两组分别称为 "手术组 (OP)+PRP" 和 "OP+PPP"。手术当天和术后第 2、4、6 和 8 天腹腔注射 PRP 或 PPP(500 μl)。认知功能通过Y迷宫、巴恩斯迷宫和被动回避测试进行评估。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组的记忆力明显下降,而 "OP+PRP "组则有明显改善。组织学分析表明,OP 组海马中神经元丢失和神经炎症增加,而 "OP+PRP "组则有所缓解。半定量分析显示,脑源性神经营养因子(BDNF)及其受体肌球蛋白受体激酶 B(TrkB)在 OP 中的表达减少,而在 "OP+PPP "中得到恢复,并在 "OP+PRP "中得到进一步改善。这些结果突显了 PRP 对 VaD 引起的海马损伤和认知障碍的保护作用,其部分原因在于 BDNF/TrkB 通路的上调。
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来源期刊
Anatomy & Cell Biology
Anatomy & Cell Biology ANATOMY & MORPHOLOGY-
CiteScore
1.80
自引率
9.10%
发文量
75
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