Calin from Hirudo medicinalis, an inhibitor of platelet adhesion to collagen, prevents platelet-rich thrombosis in hamsters
Research article published in Blood (1995)
Abstract
Interaction between exposed collagen and platelets and/or von Willebrand factor is believed to be one of the initiating events for thrombus formation at sites of damaged endothelium. Interference with this mechanism may provide an anti-thrombotic potential. Calin, a product from the saliva of the leech Hirudo medicinalis, was tested in vitro and for its in vivo activity in a thrombosis model in hamsters. Calin specifically and dose dependently (IC50:6.5 to 13 micrograms/mL) inhibited human platelet aggregation induced by collagen. In addition, specific platelet adhesion onto microtiter wells coated with collagen and detected with a monoclonal antiglycoprotein IIb/IIIa antibody-conjugated with horseradish peroxidase, could be completely prevented with Calin (IC50:22 micrograms/mL). A dose-response curve was constructed in groups of six hamsters in whom a standardized trauma was induced on the femoral vein. Thrombus formation was followed continuously using video recording and processing of the image obtained upon transillumination of the vessel. Intravenous Calin dose-dependently inhibited platelet-rich thrombus formation in this model with an ED50 of 0.07 mg/kg and complete inhibition with 0.2 mg/kg. No effects were seen on coagulation tests or bleeding times, whereas ex vivo aggregation induced by collagen was inhibited dose dependently. Local application of leech saliva, Calin, hirudin, or the combination of the latter two into the bleeding time wound of hamsters resulted in a mild prolongation of the bleeding time (twofold to threefold). A similar experiment in baboons did not cause any prolongation of the bleeding time. This is in sharp contrast with the long-lasting bleeding after a leech bite itself in both species. Calin from the leech Hirudo medicinalis is able, by binding to collagen, to effectively interfere with platelet-collagen interaction, which results in an antithrombotic effect observed in a platelet-rich thrombosis model in hamsters.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
Calin inhibits collagen-induced platelet aggregation (IC50 6.5-13 microg/mL) and prevents platelet-rich thrombosis in hamster femoral vein model with ED50 of 0.07 mg/kg.
Why This Matters for Hirudotherapy
This study examined Calin, a salivary protein from Hirudo medicinalis, both in vitro and in a hamster femoral vein thrombosis model, demonstrating dose-dependent inhibition of collagen-induced human platelet aggregation (IC50 ~6.5–13 µg/mL) and complete prevention of platelet adhesion to collagen-coated surfaces (IC50 ~22 µg/mL). Intravenous Calin dose-dependently inhibited platelet-rich thrombus formation in hamsters (ED50 ~0.07 mg/kg, complete at 0.2 mg/kg) without effects on coagulation tests or bleeding times, though local application into bleeding-time wounds mildly prolonged bleeding in hamsters but not baboons. These findings are relevant to ASH's domain as they demonstrate an in vivo antithrombotic effect of a defined leech salivary compound. The caveat is that this is an animal-model study with limited species data; the noted discrepancy between leech-bite bleeding and Calin administration effects underscores that findings may not fully represent the complete leech secretome's action in humans.
Citation
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