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Three things are happening at once: the barrier is rebuilding, an early inflammatory phase is running its course, and your pigment-producing cells are more reactive than usual

But two things are worth knowing

Research in rodent SCI models (clip compression, transection, contusion) demonstrates: Improved functional research applications (Basso-Beattie-Bresnahan locomotor rating scale scores) in BPC-157-treated animals compared to vehicle controls Reduced lesion volume at chronic timepoints, suggesting neuroprotection of spared tissue in the penumbra zone Enhanced axonal regrowth markers (GAP-43, growth-associated protein-43) in the injury zone Reduced glial scar (GFAP-positive astrocytic reactivity) at the lesion boundary a significant finding given that glial scar formation is the primary physical barrier to axonal regeneration The angiogenic mechanism of BPC-157 (VEGF stimulation, endothelial tube formation) is particularly relevant to SCI research: the spinal cord is highly vascular, and ischaemic secondary injury following disruption of spinal vasculature drives extensive secondary neurodegeneration