Intragastric Application of Aspirin, Clopidogrel, Cilostazol, and BPC 157 in Rats: Platelet Aggregation and Blood Clot.
Konosic. Sanja S; Petricevic. Mate M; Ivancan. Visnja V; Konosic. Lucija L; Goluza. Eleonora E; Krtalic. Branimir B; Drmic. Domagoj D; Stupnisek. Mirjana M; Seiwerth. Sven S; Sikiric. Predrag P
Key Findings
- BPC‑157 (10 µg/kg) given orally restored platelet aggregation that was suppressed by aspirin, clopidogrel, or cilostazol.
- The rescue effect was seen with several aggregation triggers (arachidonic acid, ADP, collagen, and arachidonic acid/PGE1).
- BPC‑157 did not alter standard clotting parameters (EXTEM, INTEM, FIBTEM, clot time, firmness, or lysis).
Practical Outcomes
- For biohackers, this suggests BPC‑157 might counteract the platelet‑inhibiting side effects of common antithrombotic drugs, but the evidence is limited to short‑term rat studies. No human dosing or safety data are available, so it isn’t ready for a DIY protocol yet, but it could be a promising area for further investigation.
Summary
In rats, giving the peptide BPC‑157 by mouth for three days helped bring back the ability of platelets to clump together even when the animals were also taking common blood‑thinning drugs like aspirin, clopidogrel, or cilostazol. The peptide didn’t change the overall clot‑forming process, just the platelet function.
Abstract
We suggest that the stable gastric pentadecapeptide BPC 157 may rescue thrombocyte function. We focused on the antithrombotic agent aspirin, clopidogrel, and cilostazol application in rats; arachidonic acid, ADP, collagen, and arachidonic acid/PGE1 platelet aggregation (aggregometry) and blood clot viscoelastic properties (thromboelastometry); and the pentadecapeptide BPC 157. Rats received intragastrically for three days once daily treatment with antithrombotic agents-aspirin (10 mg/kg) or clopidogrel (10 mg/kg) or cilostazol (10 mg/kg). Medication (BPC 157 (10 <i>μ</i>g/kg) or an equal volume of saline (5 ml/kg)) was given intragastrically, immediately after each antithrombotic agent application. For multiple electrode aggregometry and modified rotational thromboelastometry studies, blood sampling was at 2 h after last application. Adenosine diphosphate (ADP test 6.5 <i>μ</i>M), arachidonic acid (ASPI test 0.5 mM), a combination of arachidonic acid and prostaglandin E1 (ASPI test 0.5 mM and PGE1-test 30 nM), and collagen (COL test 3.2 <i>μ</i>g/ml) were used as aggregation agonists. Given with aspirin, clopidogrel, or cilostazol in rats, BPC 157 counteracted their inhibitory effects on aggregation activated by arachidonic acid, ADP, collagen, and arachidonic acid/PGE1. Specifically, this includes recovery of the aggregation induced by arachidonic acid (<i>vs.</i> aspirin, <i>vs.</i> clopidogrel, and <i>vs.</i> cilostazol), arachidonic acid/PGE1 (<i>vs.</i> cilostazol), ADP (<i>vs.</i> clopidogrel), or collagen (<i>vs.</i> clopidogrel). Contrarily, there is no effect on the used tests (extrinsic/intrinsic hemostasis system, the fibrin part of the clot) EXTEM, INTEM, and FIBTEM; clotting time; clot formation time; alpha-angle; maximum clot firmness; lysis index after 30 minutes; and maximum lysis. In conclusion, we revealed that BPC 157 largely rescues thrombocyte function.
Study Information
pubmed
2019
2019-12-30T00:00:00.000Z
10.1155/2019/9084643
52
48