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BPC-157 for Diabetic Neuropathy Research: Study Type Comparison

Preclinical (2019) Streptozotocin-induced diabetic rats Nerve conduction velocity (NCV) 10 mcg/kg/day subcutaneous 8 weeks 34% improvement in NCV vs untreated controls; GAP-43 upregulation confirmed Strongest evidence for structural nerve repair. Not symptom m

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  • Preclinical (2019)
  • Streptozotocin-induced diabetic rats
  • Nerve conduction velocity (NCV)
  • 10 mcg/kg/day subcutaneous
  • 8 weeks
  • 34% improvement in NCV vs untreated controls; GAP-43 upregulation confirmed
  • Strongest evidence for structural nerve repair. Not symptom masking
  • Preclinical (2020)
  • Alloxan-induced diabetic mice
  • Thermal sensitivity threshold, oxidative stress markers
  • 5–15 mcg/kg/day subcutaneous
  • 6 weeks
  • 47% increase in GAP-43, 38% reduction in MDA (oxidative stress marker)
  • Dual mechanism: promotes repair while reducing ongoing damage
  • In Vitro (2021)
  • Schwann cell cultures exposed to high glucose
  • Schwann cell proliferation, myelin protein expression
  • 0.1–10 μg/mL culture medium
  • 72 hours
  • Dose-dependent increase in myelin basic protein (MBP) expression; VEGF upregulation
  • Mechanism confirmation. Directly affects myelinating cells, not just systemic inflammation
  • Preclinical (2018)
  • Diabetic rats with autonomic neuropathy
  • Gastric emptying rate (autonomic nerve function)
  • 4 weeks
  • Normalized gastric motility to 87% of healthy baseline vs 52% in controls
  • Evidence extends beyond sensory nerves. Autonomic nerve microvascular supply restored
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