Pentadecapeptide BPC 157 therapy in rats with cysteamine induced-terminal ileitis

We introduce pentadecapeptide BPC 157 therapy in rats with cysteamine induced-terminal ileitis 1h/1month/2months. We counteracted gross hyperemia, edema, erosion, bleeding, microscopically significant loss of villous architecture, loss and shortening of villae and severe lymphocytic infiltrate. Pentadecapeptide counteracts various lesions in the whole GI-tract and free radical formation, and tested in ulcerative colitis trials and now in multiple sclerosis. Cysteamine was known to induce gastric-acid hypersecretion as a prototype of duodenal lesion. Cysteamine induced duodenal lesions after gastrectomy, and applied as an enema, ulcerative colitis in rats Cysteamine was applied in female Albino Wistar rats into the terminal ileum, 5 cm segment up to ileocecal valve, which was kept gently compressed for 1 min, and then released. Medication(BPC, or saline (controls)) was applied as an abdominal bath immediately after the end of the cysteamine application procedure, and then if rats were not sacrificed at 1 h, continuously, perorally in drinking water till the end of 1 or 2 months The hyperemia, edema, erosion and bleeding scores were summarized. Microscopically, cysteamine induced terminal ileitis presents with: submucosal congestion, significant loss of villous architecture, loss and shortening of villae and lamina propria infiltrated with mild to severe lymphocytic infiltrate, much like intraepithelial lymphocyte infiltration and some epithelial elevation from lamina propria. Better preservation of mucosal architecture appears in pentadecapeptide treated rats. There is only mild villous edema with capillary congestion and mild lymphocytic infiltrate. No epithelial elevation from lamina propria For further therapy, beneficial effect of the BPC counteracts cysteamine- terminal ileitis

BPC 157 given during reperfusion counteracts portal hypertension, caval hypertension, and aortal hypotension in rats with prior portal triad obstruction

Reperfusion provokes major disturbances after the Pringle maneuver. We demonstrated the usefulness of the stable gastric pentadecapeptide BPC 157 as therapy for the hemodynamic disturbances after the Pringle maneuver, a temporary portal triad obstruction (PTO) (hepatic artery, portal vein, common bile duct occlusion for 30 min), with BPC 157 given during reperfusion, in the post-PTO period. In deeply anesthetized and laparatomized rats that had a PTO, the recording lasted 5 minutes with a cannula connected to a pressure transducer, inserted into the portal vein, inferior caval vein and abdominal aorta at the level of its bifurcation at 24 h of reperfusion time. BPC 157 or saline was applied as an abdominal bath in rats that had a PTO, in the post-PTO-period, at 1 min or at 24 h reperfusion time. When BPC 157 was given in circumstances of portal and caval hypertension, and arterial hypotension, disturbances were completely eliminated. This presents a potential therapeutic advantage. Thereby, whithout therapy, the pressure of both the portal and the caval system remains elevated after removal of the portal clamp. Thus, the effectiveness of the therapy, when given at distinctive points during reperfusion, appears as conclusive evidence of its efficacy. BPC 157 therapy mitigates the whole syndrome, involving the course of an even more complex model that should include rats clamped by the hepatic artery, portal vein, and bile duct vs. rats that used to have a clamped portal triad and later underwent reperfusion

Pentadecapeptide BPC 157 counteracts portal hypertension, caval hypertension and aortal hypotension with suprahepatic occlusion of inferior caval vein in rats

Portal hypertension, aortal hypotension, caval hypertensio

Pentadecapeptide BPC 157 counteracts portal hypertension, caval hypertension and aortal hypotension with suprahepatic occlusion of inferior caval vein in rats

Portal hypertension, aortal hypotension, caval hypertensio