Published online Mar 13, 2020. doi: 10.4291/wjgp.v11.i1.1
Peer-review started: October 7, 2019
First decision: November 27, 2019
Revised: December 20, 2019
Accepted: January 19, 2020
Article in press: January 19, 2020
Published online: March 13, 2020
Processing time: 157 Days and 14 Hours
Recently, as a possible therapy resolving solution, pentadecapeptide BPC 157 therapy, has been used in alleviating various vascular occlusion disturbances. BPC 157 was previously reviewed as novel mediator of Robert cytoprotection and endothelium protection in the stomach, and gut-brain axis, beneficial therapy in gastrointestinal tract, with particular reference to vascular recruitment, ulcerative colitis and tumor cachexia, and other tissues healing. Here we raised new hypothesis about BPC 157 therapy in the Budd-Chiari syndrome in rats, rapid bypassing of the suprahepatic inferior caval vein occlusion, and rats recovery with the active and effective pharmacotherapy treatment.
To investigate Budd-Chiari syndrome model (inferior caval vein suprahepatic occlusion) resolution, since BPC 157 resolves various rat vascular occlusion.
We assessed the activated bypassing pathways between the inferior and superior caval veins and portocaval shunt, counteracted caval/portal hypertension, aortal hypotension, venous/arterial thrombosis, electrocardiogram disturbances, liver and gastrointestinal lesions (i.e., stomach and duodenum hemorrhages, in particular, congestion). Rats with suprahepatic occlusion of the inferior vena cava by ligation were medicated at 1 min, 15 min, 24 h, or 48 h post-ligation. Medication consisted of 10 µg/kg BPC 157, 10 ng BPC 157 or 5 mL/kg saline, administered once as an abdominal bath or intragastric application. Gross and microscopic observations were made, in addition to assessments of electrical activity of the heart (electrocardiogram), portal and caval hypertension, aortal hypotension, thrombosis, hepatomegaly, splenomegaly and venography. Furthermore, levels of nitric oxide, malondialdehyde in the liver and serum enzymes were determined.
BPC 157 counteracted increased P wave amplitude, tachycardia and ST-elevation, i.e., right heart failure from acute thrombotic coronary occlusion. The bypassing pathway of the inferior vena cava-azygos (hemiazygos) vein-superior vena cava and portocaval shunt occurred rapidly. Even with severe caval ˃ portal hypertension, BPC 157 antagonized portal and caval hypertension and aortal hypotension, and also reduced refractory ascites. Thrombosis of portal vein tributaries, inferior vena cava, and hepatic and coronary arteries was attenuated. In addition, there was reduced pathology of the lungs (severe capillary congestion) and liver (dilated central veins and terminal portal venules), decreased intestine hemorrhagic lesions (substantial capillary congestion, submucosal edema and architecture loss), and increased liver and spleen weight. During the period of ligation, nitric oxide- and malondialdehyde-levels in the liver remained within normal healthy values, and increases in serum enzymes were markedly reduced.
BPC 157 counteracts Budd Chiari syndrome in rats.
Core tip: To demonstrate that pentadecapeptide BPC 157 can resolve Budd Chiari syndrome in rats, we provided gross, microscopy, nitric oxide-, malondialdehyde-liver levels, serum enzymes, electrocardiogram, portal, caval hypertension, aortal hypotension, thrombosis, hepatomegaly, splenomegaly and venography assessments. BPC 157 counteracts increased P wave amplitude, tachycardia and ST-elevation (i.e., right heart failure; acute thrombotic coronary occlusion). Bypassing pathway (inferior caval vein-azygos (hemiazygos) vein-superior caval vein and portocaval shunt) rapidly appears. Even with the severe caval ˃ portal hypertension, BPC 157 counteracts portal and caval hypertension and aortal hypotension. BPC 157 counteracts refractory ascites. Portal vein tributaries, inferior caval vein, hepatic and coronary arteries thrombosis was counteracted. In addition, there are counteracted severe lung pathology, liver, intestine hemorrhagic lesion, increased liver and spleen weight. During ligation-period, nitric oxide- and malondialdehyde-level in liver remained within normal healthy values, and increased serum enzymes markedly lessened. In conclusion, BPC 157 counteracts Budd Chiari syndrome in rats.