Title:Stable Gastric Pentadecapeptide BPC 157-NO-system Relation
Volume: 20
Issue: 7
Author(s): Domagoj Drmic, Bozidar Sebecic, Hrvoje Vrcic, Senka Dzidic, Ivan Barisic, Jelena Suran, Mirjana Stupnisek, Gorana Aralica, Danijela Kolenc, Spomenko Ilic, Predrag Sikiric, Bozo Radic, Robert Klicek, Marko Sever, Luka Brcic, Dinko Stancic Rokotov, Branko Turkovic, Rudolf Rucman and Sven Seiwerth
Affiliation:
Keywords:
Arrhythmias, Chronic Heart Failure, Pentadecapeptide BPC 157, Pulmonary Hypertension, Thrombocytopenia, Thrombosis.
Abstract: We reviewed stable gastric pentadecapeptide BPC 157-NO-system-relation, its close participation in Moncada's (maintained
vascular integrity, platelets control) homeostatic healing response of NO-system to injury. Namely, BPC 157’s particular healing effect
also affects all events after vascular integrity loss (dependent on circumstances, it reduces either thrombosis (abdominal aorta anastomosis)
or bleeding/thrombocytopenia (amputation, heparin, warfarin, aspirin)) and in a series of different injurious models, acute and
chronic, BPC 157 consistently advances healing after severe injuries in various tissues spontaneously unable to heal; stimulates egr-1 and
naB2 genes; exhibits high safety (LD1 not achieved)). Hypothesis, that BPC 157 (since formed constitutively in the gastric mucosa, stable
in human gastric juice, along with significance of NO-synthase and the basal formation of NO in stomach mucosa, greater than that
seen in other tissues) exhibits a general, effective competing both with L-arginine analogues (i. e., L-NAME) and L-arginine, and that
this has some physiologic importance (NO-generation), later, practically supports its beneficial effects illustrating BPC 157 and NOsystem
mutual (with L-NAME/L-arginine; alone and together) relations in (i) gastric mucosa and mucosal protection, following alcohol
lesions, in cytoprotection course, NO-generation, and blood pressure regulation; (ii) alcohol acute/chronic intoxication, and withdrawal;
(iii) cardiovascular disturbances, chronic heart failure, pulmonary hypertension, and arrhythmias; (iv) disturbances after hypokalemia and
hyperkalemia, and potassium-cell membrane dysfunction; and finally, in (v) complex healing failure, proved by the fistulas healing,
colocutaneous and esophagocutaneous. However, how this advantage of modulating NO-system (i. e., particular effect on eNOS gene),
may be practically translated into an enhanced clinical performance remains to be determined.
