Stable gastric pentadecapeptide BPC 157 can improve the healing course of spinal cord injury and lead to functional recovery in rats.
Perovic. Darko D; Kolenc. Danijela D; Bilic. Vide V; Somun. Nenad N; Drmic. Domagoj D; Elabjer. Esmat E; Buljat. Gojko G; Seiwerth. Sven S; Sikiric. Predrag P
Key Findings
- A one‑time intraperitoneal dose of BPC‑157 (200 or 2 µg/kg) given 10 minutes after spinal cord compression improved motor function in rats.
- Histological analysis showed less axon loss, reduced edema, and fewer vacuoles and cysts in the injured spinal cord.
- Electromyography revealed lower motor unit potentials, indicating better nerve-muscle communication after BPC‑157 treatment.
- The peptide counteracted many aspects of secondary injury, such as necrosis, demyelination, and motoneuron loss.
Practical Outcomes
- For biohackers, this study suggests BPC‑157 might have neuroprotective properties that could be explored for spinal injuries or neurodegenerative conditions, but the evidence is limited to rats and a single early dose. More research, especially human trials, is needed before any safe dosing protocol can be recommended. Until then, it remains an interesting experimental lead rather than a ready‑to‑use supplement.
Summary
In a rat study, a single injection of the peptide BPC‑157 given right after a spinal cord injury helped the animals recover movement, reduced tissue damage, and improved nerve signals, suggesting the peptide may protect the spinal cord after injury.
Abstract
We focused on the therapeutic effects of the stable gastric pentadecapeptide BPC 157 in spinal cord injury using a rat model. BPC 157, of which the LD1 has not been achieved, has been implemented as an anti-ulcer peptide in inflammatory bowel disease trials and recently in a multiple sclerosis trial. In animals, BPC 157 has an anti-inflammatory effect and therapeutic effects in functional recovery and the rescue of somatosensory neurons in the sciatic nerve after transection, upon brain injury after concussive trauma, and in severe encephalopathies. Additionally, BPC 157 affects various molecular pathways. Therefore, BPC 157 therapy was administered by a one-time intraperitoneal injection (BPC 157 (200 or 2 μg/kg) or 0.9% NaCl (5 ml/kg)) 10 min after injury. The injury procedure involved laminectomy (level L2-L3) and a 60-s compression (neurosurgical piston (60-66 g) of the exposed dural sac of the sacrocaudal spinal cord). Assessments were performed at 1, 4, 7, 15, 30, 90, 180, and 360 days after injury. All of the injured rats that received BPC 157 exhibited consistent clinical improvement, increasingly better motor function of the tail, no autotomy, and resolved spasticity by day 15. BPC 157 application largely counteracted changes at the microscopic level, including the formation of vacuoles and the loss of axons in the white matter, the formation of edema and the loss of motoneurons in the gray matter, and a decreased number of large myelinated axons in the rat caudal nerve from day 7. EMG recordings showed a markedly lower motor unit potential in the tail muscle. Axonal and neuronal necrosis, demyelination, and cyst formation were counteracted. The functional rescue provided by BPC 157 after spinal cord injury implies that BPC 157 therapy can impact all stages of the secondary injury phase.
Study Information
pubmed
2019
2019-07-02T00:00:00.000Z
10.1186/s13018-019-1242-6
23
87