The Efficacy of Intrathecal Platelet-Rich Plasma Administration in Alleviation of Chronic Neuropathic Pain in Rat Model

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.