ABSTRACT
Aim: To study the effect of PLC on rabbit platelet cAMP, and then to explore the mechanism of PLC anti-aggregation to platelet. Method: Rabbit platelets removed of red cells were treated with PSS, ASA and different dose of PLC respectively and induced by ADP respectively. cAMP was extracted by trichloroacetic acid. The concentration of cAMP of differently treated platelets was determined by RIA (radioimmunoassay). Result: When rabbit platelets were treated with PSS, the concentration of cAMP at static state was 20.16 ± 0.91 pmol/109 platelets; when the platelets were treated with PSSinverted commasASA 668 μ mol·L-1, 5,10,15,20 and 25 U PLC·ml-1, the concentration of cAMP of determined at activated state induced by ADP was 13.85 ± 1.14, 16.27 ± 0.36, 18.74 ± 0.55, 19.80 ± 0.52, 20.49 ± 0.43, 22.55 ± 0.61 and 24.24 ± 0.85 (pmol/109 platelets) respectively. Compared with PSS, enhanced rates (%) of ASA 668 μmol·L-1, 5, 10, 15, 20, 25 U PLC·ml-1 to the concentration of cAMP were 17.47, 35.31, 42.96, 47.94, 62.82, 75.02 respectively. Conclusion: PLC has significant effects on the concentration of cAMP of rabbit platelets (P < 0.01), and increases cAMP dose-dependantly(P < 0.01). All these indicate PLC can enhance the concentration of cAMP. This may be one of the important reason why PLC can inhibit platelet aggregation.
ABSTRACT
Aim To study the effect of PLC on rabbit and human platelet actin polymerization, and then to explore the mechanism of PLC anti-aggregation to platelet. Methods Platelets of rabbit and human were treated with PSS, ASA and different doses of PLC respectively and then were extracted by Triton abstraction. The relative concentration of actin of differently treated platelets induced by ADP was determined by SDS-PAGE and spectrophotometre. Results For rabbit platelets were treated with PSS, the relative concentration of actin determined at static state was 1.682?0.319; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.450?0.562,1.089?0.322,1.727?0.442,1.450?0.324,1.161?0.306, 0.857?0.242 and 0.692?0.187 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.55,29.51, 40.82,52.61, 65.02,71.76 respectively.For human platelets were treated with PSS, the relative concentration of actin determined at static state was 1.358?0.376; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.445?0.750, 1.096?0.344, 1.705?0.507,1.437?0.416, 1.165?0.355, 0.845?0.257 and 0.679?0.198 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.17,30.27, 41.23,52.35, 65.44, 72.23 respectively. Conclusion PLC has significant effects on actin polymerization of rabbit and healthy human platelets (P