Peptide BPC-157 resolves inferior vena cava occlusion and Budd-Chiari syndrome in rats

The Budd-Chiari syndrome is a severe and often fatal condition characterized by the occlusion of the hepatic veins, which drain the liver. This blockage leads to a rapid increase in pressure in the veins draining the digestive system (portal hypertension) and the body's largest vein (caval hypertension), causing liver damage, fluid accumulation (ascites), and widespread thrombosis. Current therapies are often invasive and have limited efficacy in acute settings. The pentadecapeptide BPC-157 is being investigated due to its previously demonstrated benefits in protecting vascular endothelium and resolving various vascular occlusion disturbances, suggesting it may offer a novel, rapid pharmacotherapy to re-establish blood flow and mitigate the severe consequences of this syndrome.

This study used a rat model of Budd-Chiari syndrome, induced by surgical ligation of the suprahepatic inferior vena cava. Rats were treated at 1 min, 15 min, 24 h, or 48 h post-ligation. The interventions were a single dose of BPC-157 (10 µg/kg), BPC-157 (10 ng/kg), or saline (5 mL/kg) as a control, administered either as an abdominal bath or intragastrically. Researchers assessed outcomes via gross and microscopic observation, venography, electrocardiograms, and measurements of portal/caval/aortal pressures, thrombosis, organ weight, and serum/liver biomarkers like nitric oxide and malondialdehyde.

BPC-157 administration rapidly established bypassing vascular pathways, specifically the inferior vena cava-azygos vein-superior vena cava and a portocaval shunt. This counteracted the severe pathology associated with the occlusion. The peptide antagonized both portal and caval hypertension while reversing aortal hypotension. It also attenuated thrombosis in the portal vein tributaries, inferior vena cava, and hepatic and coronary arteries. Pathological changes in multiple organs were reduced, including liver damage (dilated central veins), lung congestion (severe capillary congestion), and intestinal hemorrhagic lesions. Furthermore, BPC-157 treatment normalized liver levels of nitric oxide and malondialdehyde and markedly reduced the expected increases in serum enzymes, indicating significant organ protection.

BPC-157 also counteracted electrocardiogram disturbances indicative of right heart failure from acute thrombotic coronary occlusion, including increased P wave amplitude, tachycardia, and ST-elevation.

Written by TitrateLab, separately from the study summarized above.