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膜结合补体在胶原蛋白诱导哺乳动物血小板聚集中的作用。

The role of membrane bound complement in the aggregation of mammalian platelets by collagen.

作者信息

Chater B V

出版信息

Br J Haematol. 1976 Apr;32(4):515-24. doi: 10.1111/j.1365-2141.1976.tb00954.x.

DOI:10.1111/j.1365-2141.1976.tb00954.x
PMID:1259933
Abstract

Platelets from dogs decomplemented with purified Cobra Venom Factor (CVF) lose the ability to aggregate in response to collagen stimulation. In vitro in man, dog and rabbit, and in vivo in the dog, CVF abolishes the collagen response of platelets, the effect being dose-related. Resuspension of CVF inactivated platelets in plasma containing complement resulted in a total return of sensitivity to collagen. Examination of CVF inactivated platelets with the electron microscope failed to show any marked difference from control platelets. Serotonin granules were still present and the platelets retained a discoid appearance. Incubation of platelets with antibodies to C1, C3 and C5 resulted in inhibition of the collagen response: this effect was dose-related. Light microscopy indicated that DVF does not affect the adhesion of platelets to collagen but appears to prevent subsequent aggregation. It is suggested that the complement system is involved in the induction of the platelet release reaction by collagen, and that inhibition by CVF and anticomplement antibodies is the result of a blocking of the release reaction.

摘要

用纯化的眼镜蛇毒因子(CVF)进行去补体处理的犬血小板,失去了对胶原刺激产生聚集反应的能力。在人、犬和兔的体外实验以及犬的体内实验中,CVF消除了血小板对胶原的反应,且该效应与剂量相关。将经CVF处理而失活的血小板重悬于含有补体的血浆中,其对胶原的敏感性完全恢复。用电子显微镜检查经CVF处理失活的血小板,未发现与对照血小板有任何明显差异。5-羟色胺颗粒仍然存在,且血小板保持盘状外观。用针对C1、C3和C5的抗体孵育血小板会导致胶原反应受到抑制:该效应与剂量相关。光学显微镜检查表明,CVF不影响血小板与胶原的黏附,但似乎会阻止随后的聚集。提示补体系统参与了胶原诱导的血小板释放反应,而CVF和抗补体抗体的抑制作用是释放反应受阻的结果。

相似文献

1
The role of membrane bound complement in the aggregation of mammalian platelets by collagen.膜结合补体在胶原蛋白诱导哺乳动物血小板聚集中的作用。
Br J Haematol. 1976 Apr;32(4):515-24. doi: 10.1111/j.1365-2141.1976.tb00954.x.
2
Proceedings: The role of membrane bound complement in the aggregation of mammalian platelets by collagen.论文集:膜结合补体在胶原蛋白诱导哺乳动物血小板聚集中的作用
Thromb Diath Haemorrh. 1975 Nov 15;34(2):602.
3
Human platelet-initiated formation and uptake of the C5-9 complex of human complement.人血小板启动人补体C5-9复合物的形成与摄取。
J Clin Invest. 1976 Jan;57(1):203-11. doi: 10.1172/JCI108261.
4
C1q (c1) receptor on human platelets: inhibition of collagen-induced platelet aggregation by C1q (C1) molecules.人血小板上的C1q(C1)受体:C1q(C1)分子对胶原诱导的血小板聚集的抑制作用。
J Immunol. 1976 Jul;117(1):304-9.
5
Specific interaction of HLA antibodies (eluates) with washed platelets.HLA抗体(洗脱液)与洗涤后血小板的特异性相互作用。
Br J Haematol. 1977 Mar;35(3):441-52. doi: 10.1111/j.1365-2141.1977.tb00605.x.
6
Alternate complement pathway induction of aggregation and release of 5-hydroxytryptamine and adenosine diphosphate by rabbit platelets.兔血小板通过替代补体途径诱导5-羟色胺和二磷酸腺苷的聚集与释放。
J Immunol. 1975 Feb;114(2 Pt 1):696-703.
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The effect of Trimeresurus mucrosquamatus snake venom on platelet aggregation.
Toxicon. 1978;16(6):575-82. doi: 10.1016/0041-0101(78)90185-x.
8
Clq inhibition of the interaction of collagen with human platelets.补体C1q对胶原蛋白与人类血小板相互作用的抑制作用。
J Immunol. 1976 Jan;116(1):162-3.
9
The failure to show a necessary role for C3 in the in vitro antibody response.未能证明补体3(C3)在体外抗体反应中发挥必要作用。
Eur J Immunol. 1975 Mar;5(3):185-93. doi: 10.1002/eji.1830050307.
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Trypsin-activated complex of human factor B with cobra venom factor (CVF), cleaving C3 and C5 and generating a lytic factor for unsensitized guinea pig erythrocytes. I. Generation of the activated complex.人补体B因子与眼镜蛇毒因子(CVF)的胰蛋白酶激活复合物,可裂解C3和C5,并产生针对未致敏豚鼠红细胞的溶血因子。I. 激活复合物的产生。
Biken J. 1975 Dec;18(4):193-204.

引用本文的文献

1
[Relations between complement and blood coagulation (author's transl)].补体与血液凝固之间的关系(作者译)
Klin Wochenschr. 1977 Jul 15;55(14):663-72. doi: 10.1007/BF01478832.