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Stable Gastric Pentadecapeptide BPC 157 Recovers Motor Function After Rat Spinal Cord Injury
Author(s) -
Perovic Darko,
Krezic Ivan,
Dokuzovic Stjepan,
Bilic Vide,
Gojkovic Slaven,
Drmic Domagoj,
Seiwerth Sven,
Sikiric Predrag
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.822.5
Subject(s) - medicine , spinal cord , spasticity , spinal cord injury , anesthesia , laminectomy , saline , white matter , cord , edema , surgery , magnetic resonance imaging , psychiatry , radiology
Using a well‐designed rat model, we demonstrated that the stable gastric pentadecapeptide BPC 157 improved the spinal cord injury (FASEB J 2015, 29, 617.5). Previously shown to counteract the consequence of peripheral (sciatic) nerve transection/anastomosis, and improve nerve healing (Regul Pept. 2010 Feb 25;160(1–3):33–41.), and brain trauma (Regul Pept. 2010 Feb 25;160(1–3):26–32.), and various encephalopathies (Curr Pharm Des. 2018;24(18):1990–2001), BPC 157, LD1 not achieved, was implemented as an anti‐ulcer peptide in inflammatory bowel disease trials and now in a multiple sclerosis trial(Curr Pharm Des. 2018;24(18):1990–2001). In a study from the day 1 to 1 year, rats underwent laminectomy (level L2–L3), 60 second compression (neurosurgical piston (60–66 g) on exposed dural sac with sacrocaudal spinal cord) received one medication of BPC 157 (200 or 2 μg/kg) or saline (5 ml/kg)) intraperitoneally at 10 min after injury (FASEB J 2015, 29, 617.5). All injured rats underwent BPC 157 exhibit consistent improvement, clinically, constantly better tail motor function, no autotomy; resolved spasticity already by the day 15; microscopically (since day 7), vacuolas and loss of axons in white matter, edema and loss of motoneurons in gray matter, and decrease of the number of large myelinated axons in rat caudal nerve were largely counteracted in BPC 157 rats. EMG recording evidences markedly lower MUP in tail muscle. Concluding, under the conditions of one single application, given soon after spinal cord injury, counteracted were axonal and neuronal necrosis, demyelination, cyst formation. Now, to create, however, a more reliable situation and therapy effect, the therapy with BPC 157 was started after 4 days. The medication was given in drinking water (BPC 157 10 μg/kg, 0.16 μg/mL, 12 ml/rat/day) through next 4 weeks, while controls received drinking water only. Specifically, tail motor function was scored as follows: 1 ‐ complete loss of tail function; 2 ‐ elevation maximum of 1/4 of tail length; 3 ‐ elevation maximum of 1/2 of tail; 4 ‐ elevation maximum of 3/4 of tail length; 5 – normal function. During evaluation, tail motor function score remained debilitated in rats underwent spinal cord injury that received post‐injury. Contrarily, BPC 157 treated rats exhibited huge improvement, which was continued to full recovery. Conclusion We documented that even given later after injury, the neuroprotective effect of BPC 157 quickly appears, and, BPC 157 given in drinking water, accordingly recovers the failed motor function in rats with spinal cord injury. Support or Funding Information This work was supported by the Ministry of Science, Education and Sports, Republic of Croatia [grant number 108‐1083570‐3635] . This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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