PB0908 - Therapeutic efficacy of platelet-rich plasma in chronic compression of the dorsal root ganglion in rat

Background: Chronic lower back pain with different stinging phenomena is a common symptom of lumbosacral disorders and results in functional impairment along with chronic neuropathic pain (CNP). Although platelet-rich plasma (PRP) plays an important role in modulating chronic inflammatory pain and diabetic neuropathy pain, its therapeutic efficacy in CNP is yet to be understood.

Aims: We have investigated the therapeutic efficacy of PRP administration on CNP using a chronic compression of the dorsal root ganglion (CCD) rat model.

Methods: Animals were divided into three groups: CCD, sham, and control. PRP or PBS was injected intrathecally between the L4-L5 spinal cord and alterations of behavioral responses including mechanical withdrawal threshold test, mechanical withdrawal latency test, and thermal latency test were recorded. In vivo single-unit electrophysiology recordings were obtained from the contralateral ventral posterolateral (VPL) thalamus and expression levels of specific astrocytic markers were observed by immunofluorescence.

Results: The CCD group developed a decreased pain threshold from day 7 to day 19, whereas sham and control groups showed no changes in all behavioral pain responses. Upon PRP or PBS administration for 2 weeks after day 19, the pain-related behavioral responses were improved towards pre-surgery pain threshold only in PRP-treated CCD models, but not in PBS-treated CCD models, suggesting the role of PRP in the improvement of CCD-induced CNP. Consistently, electrophysiology recording showed a significant decrease in VPL thalamic activity upon PRP administration. Moreover, immunofluorescence staining showed the ablation of pain-transmission-associated astrocyte markers including GFAP, PKM2, and HMGB1 in PRP-treated CCD models compared to PBS-treated CCD models, confirming the ability of PRP to affect the astrocyte’s activity in CNP.

Conclusion(s): We demonstrate that PRP attenuates CNP in a CCD rat model by regulating astrocytic activity associated with pain transmission, thereby providing evidence of using PRP as a promising therapeutic approach for chronic neuropathic pain in the future.