Platelet-Rich Plasma Modulates Neuroinflammation in an iPSC Model of Sensory Neurons and Microglia

Le résumé fourni par la source

Neuropathic pain (NP) is driven by neuroimmune interactions where in activated microglia release pro-inflammatory mediators that sustain central sensitization. Platelet-rich plasma (PRP) is a promising therapy, but its efficacy depends on its biochemical composition. This study aimed to evaluate how modifying the molecular profile of PRP influences its capacity to modulate neuroinflammation in a human-derived co-culture model. We compared standard PRP (sPRP) and balanced protein-concentrate plasma (BPCP), enriched in extraplatelet molecules, using an iPSC direct co-culture of sensory neurons (hSNs) and microglia (hMG). Neuroinflammation was induced for 24 h with serum-free (SF) or 10% sPRP or BPCP supplementation. Neuroinflammation, microglial activation, apoptosis, and neuronal plasticity were analyzed via RT-qPCR and Luminex. Both formulations attenuated pro-inflammatory mediators. However, BPCP demonstrated superior suppressive efficacy, reducing the levels of major cytokines (IL-1β, TNF-α, IL-6, IL-8) by half as compared to sPRP. BPCP significantly decreased IL-6, IL-8, and MCP-1 protein levels; kept microglial activation markers (CD86, CTSS) downregulated; and downregulated the apoptotic cascade (BAX, CASP9, CASP3). Conversely, sPRP displayed a distinct pro-resolving and neuroprotective trend, upregulating IL-10 and TGF-β1 and rescuing the expression of SLC12A5 (KCC2), which regulates neuronal excitability. sPRP and BPCP modulated neuroinflammation via complementary mechanisms. BPCP acted as an immunomodulatory shield suppressing macro-inflammation, while sPRP drove inflammation resolution and neuroplastic rescue.

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