Stable Gastric Pentadecapeptide BPC 157-NO-system Relation

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.

Pentadecapeptide BPC157 reduces bleeding and thrombocytopenia after amputation in rats treated with heparin, warfarin, L-NAME and L-arginine

“…Likely, this might also be the supportive part to the general interaction. Namely, very similar interactions of BPC 157 and the NO system, with both L-NAME and L-arginine, have been demonstrated by a large number of other previous studies [14,15,[18][19][20][21][22][23][24][25][26]. For instance, counteraction of both the L-arginine-induced disturbance and L-NAME-induced disturbance was seen, while maintaining blood pressure against both L-arginine (hypotension) and L-NAME (hypertension) (note, BPC 157 by itself does not affect basal blood pressure values [25] and likewise, BPC 157 by itself does not affect basal coagulation/platelets values [1]).…”

“…BPC 157 has been shown to exert beneficial effects against different pathological conditions [1,2,10-26], it induced gastroprotective, analgesic and anti-inflammatory wound healing effects [1,2,10-17], also effective against experimental colitis [10][11][12][13][14][15][16] and showing a particular interaction with the NO-system [14,15,[18][19][20][21][22][23][24][25][26]. Recently, we demonstrated the effect of BPC 157 against bleeding/thrombocytopenia after amputation, with or without anticoagulant and aspirin administration and abdominal aorta anastomotic site-thrombosis [1,2].…”

“…To counteract the consequences of L-NAME and/or L-arginine administration with the disturbed hemostasis, we administered the stable gastric pentadecapeptide BPC 157 [1,2,[10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26] not only due to its special effect on hemostasis [1,2], but also owing to a particular beneficial combining [1,2,[10][11][12][13][14], wound healing capacity [1,2,[10][11][12][13][14][15][16][17] and particular interaction with NO-system [14,15,[18][19][20][21][22][23][24][25][26]. Previously, BPC 157 as an originally anti-...…”

“…Previously, BPC 157 as an originally anti-ulcer peptide was implemented in inflammatory bowel disease trials [10][11][12][13][14][15], and now multiple sclerosis [16], lethal dose (LD1) could be not achieved [10][11][12][13][14][15][16]. As mentioned, this unusual combining effect in hemostasis was recently evidenced with bleeding/thrombocytopenia after amputation, with or without anticoagulant and aspirin administration, abdominal aorta anastomotic site-thrombosis, both being counteracted [1,2].…”

“…Wound healing capacity in different tissues [1,2,[10][11][12][13][14][15][16][17] (including blood vessels) (i.e., stimulation of the early growth response 1 (egr-1) gene and its co-repressor nerve growth factor 1-A binding protein-2 (naB2) [17] also responsible for cytokine and growth factor generation and thereby, early extracellular matrix (collagen) and blood vessel formation [17]) and endothelium protection [1,2,14,15] were implicated in these counteracting effects.…”