Platelets play a key role in the pathogenesis of atherothrombosis, and also perform the physiological hemostasis. The platelet function assays have values in the investigating patients with suspected platelet disorders and in studying the effects of anti-platelet drugs. There are increasing assays for investigating platelet function, including assessment of platelet adhesion, activation and aggregation, etc. However, all of these assays have certain limited sensitivity. It is necessary to develop a simple, sensitive assay that measures the activated platelet. This article reviewed advances of researches on platelet function assays, including assay for general function of platelet, assay of platelet adhesion function, platelet activation assay, platelet aggregation assay, platelet coagulation assay and application of flow cytometry in assessment of platelet functions, etc. and looked forward to research prospect in this field.
Blood Platelets ; physiology ; Humans ; Platelet Activation ; physiology ; Platelet Adhesiveness ; physiology ; Platelet Aggregation ; physiology ; Platelet Function Tests ; methods ; trends

OBJECTIVE: To study the effect of gradient shear stress on platelet aggregation by microfluidic chip Technology. METHODS: Microfluidic chip was used to simulate 80% fixed stenotic microchannel, and the hydrodynamic behavior of the stenotic microchannel model was analyzed by the finite element analysis module of sollidwork software. Microfluidic chip was used to analyze the adhesion and aggregation behavior of platelets in patients with different diseases, and flow cytometry was used to detect expression of the platelet activation marker CD62p. Aspirin, Tirofiban and protocatechuic acid were used to treat the blood, and the adhesion and aggregation of platelets were observed by fluorescence microscope. RESULTS: The gradient fluid shear rate produced by the stenosis model of microfluidic chip could induce platelet aggregation, and the degree of platelet adhesion and aggregation increased with the increase of shear rate within a certain range of shear rate. The effect of platelet aggregation in patients with arterial thrombotic diseases were significantly higher than normal group (P<0.05), and the effect of platelet aggregation in patients with myelodysplastic disease was lower than normal group (P<0.05). CONCLUSION The microfluidic chip analysis technology can accurately analyze and evaluate the platelet adhesion and aggregation effects of various thrombotic diseases unde the environment of the shear rate, and is helpful for auxiliary diagnosis of clinical thrombotic diseases.
Humans ; Microfluidics ; Platelet Adhesiveness ; Platelet Aggregation ; Blood Platelets/metabolism* ; Platelet Aggregation Inhibitors/pharmacology* ; Platelet Activation/physiology* ; Thrombosis

Platelet glycoprotein VI (GPVI) is a major receptor for collagen on the platelet surface. It mediates the initial platelet contact with collagen, generates intracellular signals, increases the affinity of integrin receptor, and causes platelet aggregation and thrombosis. Suppression of GPVI function can significantly inhibit collagen-induced platelet adhesion, aggregation and thrombosis, so GPVI has become a novel target for antiplatelet therapy. Within the last few years, major advances have been made in understanding platelet-collagen interactions. In this paper, the advances of study on GPVI, including composition of GPVI, functions of GPVI, factors related with functions of GPVI, GPVI and clinic were summarized.
Humans ; Platelet Adhesiveness ; physiology ; Platelet Aggregation ; physiology ; Platelet Glycoprotein GPIIb-IIIa Complex ; metabolism ; physiology ; Platelet Glycoprotein GPIb-IX Complex ; metabolism ; physiology ; Platelet Membrane Glycoproteins ; chemistry ; metabolism ; physiology ; Protein Binding ; physiology

OBJECTIVETo observe the platelet activating factor (PAF) antagonistic effect of kaempferol.

METHODThe specific binding of [3H] PAF to rabbit platelet receptor was investigatedwith radio ligand binding assay (RLBA). Platelet adhesion induced by PAF was measured with spectrophotometry. The elevation of inner free calcium concentration in rabbit polymorphonuclear leukocytes (PMNs) induced by PAF was determined with Fura-2 fluorescent technique.

RESULTThe 1, 2 or 4 nmol x L(-1) [3H]PAF specific binding to rabbit platelet receptor was inhibited by Kae dosage dependently and the IC50 were 30.8, 74.6 and 92.0 micro mol x L(-1), respectively. The PAF induced reactions of rabbit platelet adhesion and PMNs inner free calcium concentration elevation were inhibited by Kae in a dose-dependent manner. The IC50 of Kae to inhibit platelet adhesion was 65 micromol x L(-1).

CONCLUSIONKae is effective in inhibiting the action of PAF and it is a new PAF receptor antagonist.

Animals ; Blood Platelets ; drug effects ; physiology ; Calcium ; metabolism ; Kaempferols ; pharmacology ; Male ; Neutrophils ; metabolism ; Platelet Activating Factor ; metabolism ; Platelet Adhesiveness ; drug effects ; Platelet Membrane Glycoproteins ; antagonists & inhibitors ; metabolism ; Rabbits ; Radioligand Assay ; Receptors, G-Protein-Coupled ; antagonists & inhibitors ; metabolism

OBJECTIVE: To explore the main factors of platelet spreading and provide the foundation for related research. METHODS: Platelets (2×10⁷/ml) were draw from C57BL/6J mouse and kept at 22 ℃ for 1-2 hours. Platelets (2×10⁷/ml) were were allowed to adhere and spread on the fibrinogen-coated slides, after staining F-actin in platelets, the platelets were observed with the confocal microscopy. The effects of different concentrations of fibrinogen (10 μg/ml, 30 μg/ml, 100 μg/ml) and kinds of agonists ［thrombin(0.01,0.05,0.1 U/ml), ADP（5,10,20 μmol/L）, U46619（0.125,0.25,0.5 μmol/L）］ on platelets were analyzed. The platelet spreading was successful if the spreading rate was higher after treated with agonists. RESULTS: Compared to the group which coated with 10 μg/ml and 100 μg/ml fibrinogen, the platelet density is optimal when coated with 30 μg/ml fibrinogen. In addition, under the stimulation of thrombin, ADP and U46619, the spreading rate of platelets showed a certain concentration-dependent increasing. CONCLUSION The platelet spreading is easily influenced by various factors, the platelet spreading can be induced successfully at 0.1 U/ml thrombin, 20 μmol/L ADP and 0.5 μmol/L U46619 on the slide coated with 30 μg/ml fibrinogen.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology* ; Adenosine Diphosphate ; Animals ; Blood Platelets/physiology* ; Fibrinogen ; Humans ; Mice ; Mice, Inbred C57BL ; Platelet Adhesiveness/physiology* ; Thrombin/pharmacology*