Nikhil Prasad Fact checked by:Thailand Medical News Team Aug 09, 2026 42 minutes ago
Neuropathic pain can be extremely difficult to treat because the problem involves much more than damaged or overactive nerves. New laboratory research suggests that specially modifying platelet-rich plasma, or PRP, could potentially influence the inflammatory processes that help keep this type of chronic pain alive.
Modified platelet-rich plasma showed powerful effects on inflammation and nerve-related pathways linked to
neuropathic pain in a human cell model
Researchers compared standard platelet-rich plasma (sPRP) with a modified formulation called balanced protein-concentrate plasma (BPCP). The latter contains increased concentrations of important molecules found in plasma outside platelets. Both formulations reduced signs of inflammation, but they appeared to work through surprisingly different biological pathways.
Researchers Created a Human Nerve-Immune Model
The researchers were Jon Mercader-Ruiz, Daniel Marijuan-Pinel, Diego Delgado, Deiene Lasuen Aguirre, Xabier Sansinanea, Jorge Guadilla and Mikel Sánchez. Their institutions were the Advanced Biological Therapy Unit, MiKS Hospital, Vitoria-Gasteiz, Spain, and the Arthroscopic Surgery Unit, MiKS Hospital, Vitoria-Gasteiz, Spain. Genetic and cellular analyses were also performed using the Genetics, Epigenetics, and Cellular Biology platform of Bioaraba Health Research Institute, Vitoria-Gasteiz, Spain.
The scientists created a laboratory model combining human sensory neurons with microglia derived from induced pluripotent stem cells. Microglia are immune-like cells of the nervous system that can become activated after nerve injury and release inflammatory chemicals that increase nerve sensitivity.
The cells were deliberately exposed to inflammatory substances before receiving either standard PRP or BPCP.
Modified PRP Produced Stronger Inflammatory Suppression
Both treatments reduced major inflammatory signals, including IL-1β, TNF-α, IL-6 and IL-8. However, BPCP produced broader suppression. Gene expression of these four major inflammatory cytokines was reduced by at least half compared with standard PRP.
Protein measurements supported these findings. BPCP produced significantly greater reductions in IL-6, IL-8 and MCP-1 than standard PRP. MCP-1 is particularly important because it helps recruit and activate immune cells, potentially contributing to continuing inflammation.
Importantly, the two preparations contained similar platelet concentrations. This suggests that BPCP's stronger effects may have resulted from its increased concentration of molecules in the plasma itself rather than simply having more platelets.
As highlighted in this
Thailand Medical News report, the findings challenge the idea that platelets alone determine PRP's biological effects.
The Two Plasma Treatments Worked Differently
BPCP kept important microglial activation markers, including CD86 and CTSS, relatively low. It also suppressed genes involved in
apoptosis, the controlled process through which damaged or stressed cells initiate cellular death.
Standard PRP showed a different pattern. Rather than producing the same broad suppression, it increased signals associated with resolving inflammation, particularly IL-10 and TGF-β1.
Standard PRP also showed potentially important effects on neuronal function. It partially restored expression of SLC12A5, the gene encoding the KCC2 transporter. Reduced KCC2 activity is associated with abnormal neuronal excitability and mechanisms contributing to neuropathic pain.
Another intriguing result involved MMP-9. BPCP produced roughly twice the MMP-9 protein response seen with standard PRP. MMP-9 can contribute to inflammation and pain under some circumstances but can also participate in tissue remodeling, nerve regeneration and remyelination, meaning this finding requires careful interpretation.
Important Limitations Remain
The research was conducted in laboratory-grown cells rather than patients. The model also used cells derived from a single donor, and functional experiments had a relatively small sample size. Therefore, the findings do not establish that either PRP formulation can relieve neuropathic pain in humans.
Conclusions
The study suggests that PRP composition could matter considerably when developing treatments for neuropathic pain. BPCP appeared better at broadly suppressing inflammation and apoptosis, while standard PRP showed stronger inflammation-resolving and neuroplastic effects. These complementary actions raise the possibility that future PRP therapies could eventually be customized according to the biological mechanisms driving an individual patient's pain.
The study findings were published in the peer reviewed journal: International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/16/7127 
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