Protective effects of BPC 157 in rats with experimentally induced lower extremity ischemia-reperfusion injury

In a rat model of lower-limb ischemia-reperfusion injury, treatment with BPC 157 reduced markers of oxidative stress and apoptosis, dampened inflammation, and partially restored pro-angiogenic signaling. The study randomized 24 male Wistar albino rats to sham, BPC-only, ischemia-reperfusion, or ischemia-reperfusion plus BPC groups, and compared serum, gene-expression, immunohistochemical, and histological measures. These results support BPC 157 as a candidate for further study in reperfusion injury, but not as a proven clinical treatment.

Journal article — randomized controlled animal study. Population: Male Wistar albino rats with experimentally induced lower extremity ischemia-reperfusion injury. Sample size: 24 male Wistar albino rats. Follow-up: 45 minutes of ischemia followed by 2 hours of reperfusion. Interventions: BPC 157 (20 µg/kg, intraperitoneal).

In this model, 45 minutes of abdominal aortic clamping followed by 2 hours of reperfusion significantly increased MDA, TOS, p53, Bax, Casp3, Hif-1α, Il-6, and histopathological injury scores, and reduced SOD, TAS, and VEGF expression versus SHAM. BPC 157 at 20 µg/kg significantly raised Bcl-2 expression versus IR and reduced MDA and TOS, restored SOD and TAS, downregulated p53, Bax and Casp3, lowered IL-6 and Caspase-3 immunoreactivity, and partially restored VEGF. Histology showed improved muscle architecture and less collagen deposition in the IRB group than in the IR group. Bcl-2 mRNA was not significantly reduced by I/R versus SHAM.

This paper provides mechanistic rat-model evidence that BPC 157 attenuates oxidative stress, apoptosis, and inflammation while supporting angiogenic activity in skeletal muscle after ischemia-reperfusion. For BPC-157 researchers, it supports further investigation in lower-extremity reperfusion injury, but it does not establish clinical efficacy, safety, or dosing in humans.

Key findings

Compared with SHAM, I/R significantly increased MDA, TOS, p53, Bax, Casp3, Hif-1α, Il-6, and histopathological injury scores while reducing SOD, TAS, and VEGF expression.
BPC 157 significantly increased Bcl-2 expression compared with the IR group, although Bcl-2 mRNA was not significantly reduced by I/R versus SHAM.
In I/R rats, BPC 157 reduced MDA and TOS, restored SOD and TAS, downregulated p53, Bax and Casp3, and reduced IL-6 and Caspase-3 immunoreactivity.
BPC 157 partially restored VEGF expression and improved muscle architecture with reduced collagen deposition versus IR.
BPC 157 was given intraperitoneally at 20 µg/kg at the 45th minute of ischemia.

Limitations

Authors state that larger cohorts and dose-response evaluations are needed to confirm these effects and establish clinical relevance.
Small group sizes (n = 6) limit precision and generalizability.
Only a single 2-hour reperfusion window was assessed, so longer-term outcomes remain unknown.
Findings from a rat model may not translate to human disease.

The record

Journal: Scientific reports 16(1): 24375
Published: 2026-05-28
PMID: 42204242 — DOI: 10.1038/s41598-026-55449-1
MeSH terms: Lower Extremity, Animals, Rats, Rats, Wistar, Reperfusion Injury, Disease Models, Animal, Peptide Fragments, Protective Agents, Apoptosis, Oxidative Stress, Male, Caspase 3, Biomarkers
Author countries: Turkey

Peptide profiles: BPC-157.

All indexed evidence: BPC-157 trials & papers.