Pentadecapeptide BPC 157 and anaphylactoid reaction in rats and mice after intravenous dextran and white egg administration

Duplančić, Božidar; Stambolija, Vasilije; Holjevac, Jadranka Katancic; Zemba, Mladen; Balenovic, Igor; Drmic, Domagoj; Šuran, Jelena; Radic, Bozo; Filipović, Marinko; Blagaić, Alenka Boban; Brčić, Luka; Kolenc, Danijela; Grabarević, Željko; Seiwerth, Sven; Sikirić, Predrag

doi:10.1016/j.ejphar.2014.01.046

Cited by 9 publications

(6 citation statements)

References 23 publications

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“…These lesions could be all influenced by the NOS substrate L-arginine and in particular by the stable pentadecapeptide BPC 157, which is an agent known to counteract non-selective NSAID-induced ulcerogenesis as well as the liver and brain lesions that interact with the NO system[ 1 , 9 ]. The additional support comes from the similar therapy effects obtained with the correspondingly high dose range of BPC 157 therapy, which was similar to the dosing used in other studies as well[ 33 , 34 ].…”

Section: Discussionsupporting

confidence: 66%

Celecoxib-induced gastrointestinal, liver and brain lesions in rats, counteraction by BPC 157 or L-arginine, aggravation by L-NAME

Drmic¹,

Kolenc²,

Ilic³

et al. 2017

WJG

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AIMTo counteract/reveal celecoxib-induced toxicity and NO system involvement.METHODSCelecoxib (1 g/kg b.w. ip) was combined with therapy with stable gastric pentadecapeptide BPC 157 (known to inhibit these lesions, 10 μg/kg, 10 ng/kg, or 1 ng/kg ip) and L-arginine (100 mg/kg ip), as well as NOS blockade [N(G)-nitro-L-arginine methyl ester (L-NAME)] (5 mg/kg ip) given alone and/or combined immediately after celecoxib. Gastrointestinal, liver, and brain lesions and liver enzyme serum values in rats were assessed at 24 h and 48 h thereafter.RESULTSThis high-dose celecoxib administration, as a result of NO system dysfunction, led to gastric, liver, and brain lesions and increased liver enzyme serum values. The L-NAME-induced aggravation of the lesions was notable for gastric lesions, while in liver and brain lesions the beneficial effect of L-arginine was blunted. L-arginine counteracted gastric, liver and brain lesions. These findings support the NO system mechanism(s), both NO system agonization (L-arginine) and NO system antagonization (L-NAME), that on the whole are behind all of these COX phenomena. An even more complete antagonization was identified with BPC 157 (at both 24 h and 48 h). A beneficial effect was evident on all the increasingly negative effects of celecoxib and L-NAME application and in all the BPC 157 groups (L-arginine + BPC 157; L-NAME + BPC 157; L-NAME + L-arginine + BPC 157). Thus, these findings demonstrated that BPC 157 may equally counteract both COX-2 inhibition (counteracting the noxious effects of celecoxib on all lesions) and additional NOS blockade (equally counteracting the noxious effects of celecoxib + L-NAME).CONCLUSIONBPC 157 and L-arginine alleviate gastrointestinal, liver and brain lesions, redressing NSAIDs’ post-surgery application and NO system involvement.

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Section: Discussionsupporting

confidence: 66%

Celecoxib-induced gastrointestinal, liver and brain lesions in rats, counteraction by BPC 157 or L-arginine, aggravation by L-NAME

Drmic¹,

Kolenc²,

Ilic³

et al. 2017

WJG

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“…Together, these findings indicate that with regard to wounds in operating instances, a BPC 157–defensive system exists that may accommodate the healing depending on the tissue and injury conditions. Of note, the possible contribution of the particular counteracting effect on the intravenous dextran- or egg white–induced anaphylactoid reaction ( Duplancic et al, 2014 ) should also be considered, although not specifically mentioned in this review. Unlike histamine receptor antagonists (H1 and H2), BPC 157 has a strong beneficial effect in both rats and mice.…”

Section: Discussionmentioning

confidence: 99%

“…Upper and lower lip and snout edema, as well as extreme cyanosis and edema of paws and scrotum were markedly attenuated. Poor respiration and fatalities were not observed ( Duplancic et al, 2014 ). However, it remains to be seen when this particular balanced modulatory action will have further application in therapy.…”

Section: Discussionmentioning

confidence: 99%

Stable Gastric Pentadecapeptide BPC 157 and Wound Healing

et al. 2021

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Significance: The antiulcer peptide, stable gastric pentadecapeptide BPC 157 (previously employed in ulcerative colitis and multiple sclerosis trials, no reported toxicity (LD1 not achieved)), is reviewed, focusing on the particular skin wound therapy, incisional/excisional wound, deep burns, diabetic ulcers, and alkali burns, which may be generalized to the other tissues healing.Recent Advances: BPC 157 has practical applicability (given alone, with the same dose range, and same equipotent routes of application, regardless the injury tested).Critical Issues: By simultaneously curing cutaneous and other tissue wounds (colocutaneous, gastrocutaneous, esophagocutaneous, duodenocutaneous, vesicovaginal, and rectovaginal) in rats, the potency of BPC 157 is evident. Healing of the wounds is accomplished by resolution of vessel constriction, the primary platelet plug, the fibrin mesh which acts to stabilize the platelet plug, and resolution of the clot. Thereby, BPC 157 is effective in wound healing much like it is effective in counteracting bleeding disorders, produced by amputation, and/or anticoagulants application. Likewise, BPC 157 may prevent and/or attenuate or eliminate, thus, counteract both arterial and venous thrombosis. Then, confronted with obstructed vessels, there is circumvention of the occlusion, which may be the particular action of BPC 157 in ischemia/reperfusion.Future Directions: BPC 157 rapidly increases various genes expression in rat excision skin wound. This would define the healing in the other tissues, that is, gastrointestinal tract, tendon, ligament, muscle, bone, nerve, spinal cord, cornea (maintained transparency), and blood vessels, seen with BPC 157 therapy.

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“…Endothelium protection [ 14 - 21 ] leads to its particular effect on arterial thrombosis, counteraction of prolonged bleeding after amputation and anticoagulants administration [ 24 , 48 ], as well as NO-substrate and NOS-blocker administration, and opposite conditions arising from NO-system overstimulation or blockade [ 48 ], and finally, rescue of animals with a major vein obstruction (inferior caval vein) [ 49 ]. Likely, this effect could be responsible for the counteracted dextran-induced anaphylactoid reaction and increased vascular permeability [ 50 ]. Also, BPC 157 exerts a particular beneficial effect on chronic heart failure induced by doxorubicin and arrhythmias induced by digitalis as well as hyperkalemia and potassium-induced membrane disturbances [ 51 - 53 ].…”

Section: Bpc 157 In Periphery-biological Actions and Significance Formentioning

confidence: 99%

Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications

Sikirić

Seiwerth²,

Rucman³

et al. 2016

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BackgroundBrain-gut interaction involves, among others, peptidergic growth factors which are native in GI tract and have strong antiulcer potency and thus could from periphery beneficially affect CNS-disorders. We focused on the stable gastric pentadecapeptide BPC 157, an antiulcer peptidergic agent, safe in inflammatory bowel disease trials and now in multiple sclerosis trial, native and stable in human gastric juice.MethodsReview of our research on BPC 157 in terms of brain-gut axis.ResultsBPC 157 may serve as a novel mediator of Robert’s cytoprotection, involved in maintaining of GI mucosa integrity, with no toxic effect. BPC 157 was successful in the therapy of GI tract, periodontitis, liver and pancreas lesions, and in the healing of various tissues and wounds. Stimulated Egr-1 gene, NAB2, FAK-paxillin and JAK-2 pathways are hitherto implicated. Initially corresponding beneficial central influence was seen when BPC 157 was given peripherally and a serotonin release in particular brain areas, mostly nigrostriatal, was changed. BPC 157 modulates serotonergic and dopaminergic systems, beneficially affects various behavioral disturbances that otherwise appeared due to specifically (over)stimulated/damaged neurotransmitters systems. Besides, BPC 157 has neuroprotective effects: protects somatosensory neurons; peripheral nerve regeneration appearent after transection; after traumatic brain injury counteracts the otherwise progressing course, in rat spinal cord compression with tail paralysis, axonal and neuronal necrosis, demyelination, cyst formation and rescues tail function in both short-terms and long-terms; after NSAIDs or insulin overdose or cuprizone encephalopathies were attenuated along with GI, liver and vascular injuries.ConclusionBPC 157, a gastric peptide, may serve as remedy in various CNS-disorders.

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Pentadecapeptide BPC 157 and anaphylactoid reaction in rats and mice after intravenous dextran and white egg administration

Cited by 9 publications

References 23 publications

Celecoxib-induced gastrointestinal, liver and brain lesions in rats, counteraction by BPC 157 or L-arginine, aggravation by L-NAME

Celecoxib-induced gastrointestinal, liver and brain lesions in rats, counteraction by BPC 157 or L-arginine, aggravation by L-NAME

Stable Gastric Pentadecapeptide BPC 157 and Wound Healing

Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications

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