Endothelium-Dependent Nitric Oxide-Mediated Vasorelaxant Effects of BPC 157 in Human Internal Mammary Artery.
This study investigated whether the synthetic peptide BPC 157 (Body Protection Compound-157) could relax human arterial tissue and whether that effect depends on the endothelium and nitric oxide (NO) signaling. Researchers used residual segments of internal mammary artery (IMA) collected from 12 patients undergoing elective coronary artery bypass graft surgery. Arterial rings were prepared with the endothelium either intact or deliberately removed, then pre-contracted with phenylephrine. Cumulative doses of BPC 157 were applied, and separate experiments used the NOS inhibitor L-NAME to assess NO involvement. The study found that BPC 157 produced a concentration-dependent reduction in arterial contraction in both endothelium-intact and endothelium-denuded rings, but relaxation was significantly greater when the endothelium was present. L-NAME pre-treatment blunted the relaxation response, implicating the endothelial NO pathway as the primary mechanism. Residual relaxation in denuded rings suggested that additional, endothelium-independent mechanisms also contribute. The authors acknowledge limitations including the small sample size (n = 12), the ex vivo nature of the tissue model, and the absence of in vivo or molecular mechanistic data, calling for further research before clinical conclusions can be drawn.
Why this grade: Although human tissue (IMA rings from n=12 patients) was used, this is a small-sample ex vivo pharmacological study with no in vivo administration to human subjects, limiting the strength of clinical inference.
Background/Objectives: Body Protection Compound-157 (BPC 157) is a stable gastric pentadecapeptide with cytoprotective, pro-angiogenic, and nitric oxide (NO)-modulating properties that has gained increasing attention for its therapeutic potential. Although vasodilatory effects have been demonstrated in animal models, functional evidence in human arterial tissue remains limited. This study investigated the effects of BPC 157 on vascular tone in human internal mammary artery (IMA) rings and evaluated the contribution of endothelial NO signaling. Methods: Residual IMA segments obtained from elective coronary artery bypass graft surgeries ( n = 12) were dissected into endothelium-intact and endothelium-denuded rings. Following equilibration, the rings were challenged by phenylephrine (PheE; 3 × 10 -6 M) to induce contraction. Cumulative concentration-response curves of BPC 157 (0.01-1 mg/mL) for five consecutive doses were constructed. The involvement of NO was assessed by BPC 157 dose-response curves in the nitric oxide synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME; 10 -6 M) pre-incubated rings. Maximum force of contraction, area under the curve, maximum response (Emax), and negative logarithm of the half-maximal effective concentration (pEC50) values were analyzed. Results: BPC 157 produced a concentration-dependent reduction in PheE-induced contraction in both groups, with significantly greater relaxation in endothelium-intact rings ( p Conclusions: BPC 157 induces concentration-dependent vasorelaxation in human arterial tissue, predominantly mediated via an endothelium-dependent NO pathway. Endothelial integrity primarily enhances maximal efficacy, while residual effects indicate additional mechanisms. These findings provide early mechanistic evidence for the vascular activity of BPC 157, although further molecular and in vivo studies are required to clarify its clinical relevance.
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