Duodenocolic fistula healing by pentadecapeptide BPC 157 in rats. A cytoprotection viewpoint.
Vukusic. D D; Zenko Sever. A A; Sever. M M; Drmic. D D; Milavic. M M; Sikiric. S S; Rasic. D D; Krezic. I I; Gojkovic. S S; Prtoric. A A; Bubalo. P P; Coric. L L; Dobric. I I; Boban Blagaic. A A; Rasic. Z Z; Skrtic. A A; Seiwerth. S S; Sikiric. P P
Key Findings
- Local or oral BPCâ157 (10âŻÂ”g/kg) caused rapid recruitment of tiny blood vessels to both sides of the fistula.
- All treated rats healed the duodenal and colonic defects, kept their weight, had no diarrhea, and showed far fewer adhesions compared with controls.
- Gene expression shifted: strong increase in iNOS and decreases in COXâ2, VEGFâA, NOSâ1, NOSâ3, and NFâÎșBâactivating protein.
Practical Outcomes
- The study suggests that a low oral dose of BPCâ157 may be enough to promote healing of severe gastrointestinal injuries. For biohackers, this points to the possibility of using oral BPCâ157 (â10âŻÂ”g per kg body weight) to support gut repair, but human trials are still needed and safety/efficacy in people remain unproven.
Summary
In rats with a serious gut leak (a duodenocolic fistula), giving the peptide BPCâ157 either directly at the wound or by mouth quickly pulled new tiny blood vessels to the damage, closed the hole, and prevented weight loss, diarrhea, and scar tissue. The drug also changed several healingârelated genes. While the work is in animals, it shows that lowâdose oral BPCâ157 can dramatically speed up gut repair.
Abstract
Using duodenocolic fistula in rats, this study attempts to highlight the particular cytoprotection aspects of the healing of fistulas and therapy potential of the stable gastric pentadecapeptide BPC 157, a cytoprotection mediator (i.e. upgrading minor vessels to induce healing at both fistula's sides). Upon duodenocolic fistula creation (two 'perforated' lesions put together) (assessed at 3, 6, 9, 12, and 15 min), BPC 157, given locally at the fistula, or intragastrically (10 μg/kg, 10 ng/kg), rapidly induces vessel 'recruitment', 'running' toward the defect, simultaneously at duodenum and colon, providing numerous collaterals and branching. The mRNA expression studies done at that time provided strongly elevated (nitric oxide synthase 2) and decreased (cyclooxygenase-2, vascular endothelial growth factor A, nitric oxide synthase (NOS)-1, NOS-3, nuclear factor-kappa-B-activating protein) gene expression. As therapy, rats with duodenocolic fistulas, received BPC 157 10 μg/kg, 10 ng/kg, per-orally, in drinking water till sacrifice, or alternatively, intraperitoneally, first application at 30 min after surgery, last at 24 h before sacrifice, at day 1, 3, 7, 14, 21, and 28. Controls exhibited both defects persisting, continuous fistula leakage, diarrhea, continuous weight loss, advanced adhesion formation and intestinal obstruction. Contrary, all BPC 157-treated rats have closed both defects, duodenal and colonic, no fistula leakage (finally, maximal instilled volume corresponds to healthy rats), no cachexia, the same weight as before surgery, no diarrhea, markedly less adhesion formation and intestinal passage obstruction. Thus, BPC 157 regimens resolve the duodenal/colon lesions and duodenocolic fistulas in rats, and rapid vessels recovery appears as the essential point in the implementation of the cytoprotection concept in the fistula therapy.
Study Information
pubmed
2024
2024-04-03T00:00:00.000Z
10.26402/jpp.2024.1.09
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