Cytoprotective gastric pentadecapeptide BPC 157 resolves major vessel occlusion disturbances, ischemia-reperfusion injury following Pringle maneuver, and Budd-Chiari syndrome

Core Tip

Core Tip: Summarizing the essential epithelium and endothelium protection interplay described in Robert’s and Szabo’s cytoprotection concept, and the role of the stable pentadecapeptide BPC 157 as a likely mediator, we suggest that BPC 157 may be a useful cytoprotective therapy. The hope is that it could finally bring into practice the huge theoretical importance of all aspects of the cytoprotection concept. Conceptually, there is a new point to discuss, namely, endothelium maintenance to epithelium maintenance (recruitment of collateral blood vessels to compensate for vessel occlusion and reestablish blood flow or bypass the occluded or ruptured vessel). BPC 157 counteracts various venous occlusion-induced syndromes, as well as inferior caval vein syndrome, ischemia-reperfusion injury following Pringle maneuver, and Budd-Chiari syndrome in rats. Activation of the alternative collateral pathways to bypass occlusion and reestablish alternative blood flow, results in the counteraction of the consequent syndromes. The severe venous occlusion-induced disturbances, the high portal and caval hypertension, aortal hypotension, arterial and venous thrombosis, both peripherally and centrally, and various organ lesions (i.e., gastrointestinal, liver, kidney, heart, and brain) were all attenuated and/or eliminated. Furthermore, this particular beneficial effect may be competing with the Virchow's triad that can be a common presentation [i.e., duodenal venous congestion lesions, perforated cecum, ischemic/reperfusion colitis, bile duct ligation-induced liver cirrhosis and portal hypertension, temporary portal triad occlusion (ischemia-reperfusion injury following the Pringle maneuver), and suprahepatic occlusion of the inferior caval vein (Budd-Chiari syndrome)]. The resolution of these various venous occlusion-induced syndromes emphasizes the evidence that as the native cytoprotective gastric peptide and a stable gastric pentadecapeptide membrane stabilizer, BPC 157, which is stable in the human gastric juice and counteracts gut-leaky syndrome, is a particular target and easily distinguished from standard peptide growth factors, involving particular molecular pathways, and specifically controlling the VEGF and NO pathways, in particular the prostaglandin pathway.