Anti-platelet-aggregation polypeptide

Abstract

The invention discloses an anti-platelet-aggregation polypeptide, belongs to the field of medical biotechnology, and in particular relates to a novel polypeptide having the function of inhibiting platelet aggregation. The polypeptide is a polypeptide KM6 consisting of 10 amino acids, having a sequence of SEQ ID NO: 1, and having a molecular weight of 1103. 19 Da, and the sequence of the polypeptide KM6 is Gln-Leu-Ser-Asn-Gly-Asn-Arg-Thr-Leu-Thr. The polypeptide has obvious inhibitory effects on collagen, ADP, arachidonic acid and thrombin-induced platelet aggregation, can be used for exploringthe influence of the polypeptide KM6 and other platelet activators (such as epinephrine and ristomycin) on the effect and related functions of platelets, and can also be used to monitor existing antiplatelet therapies.

Description

technical field [0001] The invention belongs to the technical field of medicine and biology, and in particular relates to a new polypeptide with the function of inhibiting platelet aggregation. Background technique [0002] Cardiovascular and cerebrovascular diseases mainly include acute myocardial infarction, cerebral infarction, pulmonary infarction, ischemic heart disease, stroke and other common diseases, which seriously threaten human health and life and are the first cause of death among Chinese residents [1]. Platelet activation is an important initiating factor in the occurrence and development of cardiovascular and cerebrovascular diseases, and platelet activation, adhesion and aggregation to thrombus formation are a series of cascade reactions, which not only play a key role in the physiological hemostasis process, but also Participate in pathological processes such as thrombosis and tissue repair[2,3]. Platelet aggregation plays a central role in thrombus formati...

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Problems solved by technology

[0011] However, the existing antiplatelet drugs not only have side effects such as bleeding tendency (cerebral hemorrhage, gastrointestinal hemorrhage) [21], but also have resistance or low response in clinical application, and adverse ischemic events still occur; at the same time, the effects of these drugs The mechanism is single, and the antiplatelet effect has certain limitations: for example, aspirin irreversibly blocks the synthesis of COX-1, thereby inhibiting platelet activation and aggregation[10,22]; clopidogrel irreversibly inhibits the binding of ADP to its receptor P2Y12, and inhibits the induction of ADP platelet aggregation[23]; ticagrelor reversibly interacts with the ADP-P2Y12 receptor, and also inhibits ADP-induced platelet aggregation[24]; Vorapaxar and Atopaxar are PAR-1 inhibitors currently in clinical trials, which can Inhibit thrombin-induced platelet aggregation[25,26]; Abciximab, tirofiban, and eptifibatide are all GPⅡb / Ⅲa receptor antagonists[27]

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