ArticleMolecular neurobiology2025
The Efficacy of Intrathecal Platelet-Rich Plasma Administration in Alleviation of Chronic Neuropathic Pain in Rat Model.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Platelet-Rich Plasma Modulates Neuroinflammation in an iPSC Model of Sensory Neurons and Microglia.International journal of molecular sciences · 2026Article
- The potential of platelet-rich plasma and PRP-derived biologics for neurological disorders: mechanisms and translational research.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Chronic neuropathic pain (CNP), marked by various stinging sensations, frequently arises from lumbosacral disorders, where astrocytes in the spinal dorsal horn (SDH) significantly contribute to its persistence. Platelet-rich plasma (PRP) treatment has shown regulatory effects on astrocytic activity in inflammatory and diabetic neuropathy, yet its impact on CNP remains unclear. This study investigates the potential of intrathecal PRP injections for mitigating CNP in a chronic compressed dorsal root ganglion (CCD) rat model. Animals were divided into CCD, sham, and control groups. PRP or phosphate-buffered saline (PBS) was injected intrathecally between the L4-L5 spinal cord. Assessments included mechanical and thermal pain behavioral tests, and in vivo extracellular recordings from the contralateral ventral posterolateral (VPL) thalamus. Additionally, the expression of astrocytic pain mediators in the SDH was analyzed through immunofluorescence. Results showed that the CCD group had significantly lower pain thresholds compared to the sham group. PRP treatment led to improved CNP responses in CCD rats, unlike in the PBS group, highlighting PRP's role in CNP amelioration. Electrophysiology confirmed a notable reduction in VPL thalamic activity post-PRP treatment. Immunofluorescence (IFC) analysis revealed significant increases in neuronal c-fos expression in the DRG and SDH of CCD rats, which were notably reduced following PRP treatment. IFC analysis also indicated decreased expression of pain-transmission-associated astrocyte markers, including glial fibrillary acidic protein (GFAP), pyruvate kinase M2 (PKM2), and high mobility group box-1 protein (HMGB1) in PRP-treated CCD subjects. Thus, we demonstrate that PRP attenuates CNP in a CCD rat model by regulating nociceptive input into the spinothalamic tract through the inhibition of astrocytic activity in SDH, presenting itself as a viable therapy for CNP linked to lumbosacral conditions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.