ABSTRACT
Objective To study the anticoagulant and fibrinolytic mechanism of vascular endothelial cells in rabbit model of blood stasis syndrome (BSS). Methods BS S rabbit model was induced by injection of noradrenaline and bovine serum albumin . The aortic endothelial cells from the normal rabbits (Group A)and BSS rabbits (Group B)were cultured primarily and subcultured. The activities of antithrombin Ⅲ (AT_Ⅲ), tis sue_type plasminogen activator (t_PA) and plasminogen activator inhibitor (PAI) in the plasma of rabbits and cultured supernatant were measured. Results The activities of t_PA and AT_Ⅲ were obviously decreased and PAI activity incre ased in the plasma of BSS model rabbits as compared with those of the normal rabbits (P 0.05 ). Conclusion Anticoagulant and fibrinolytic dysfunction p lays an imp ortant role in the occurrence and development of BSS.
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Objective To explore the molecular mechanism of blood_stasis syndrome (BSS) by studying the changes of gene expression of endothelin (ET) and constit utive nitric oxide synthase (cNOS) in vascular endothelial cells (VEC) cultured w ith BSS rabbit serum. Methods ET_1 mRNA expression and cNOS mRNA expression were analyzed by semi_quantitative reverse transcription and polymerase chain re action method. Results ET_1 mRNA expression level was increased and cNOS mRN A expression level was decreased in VEC cultured with BSS rabbit serum (Group A) as compared with VEC cultured with normal rabbit serum (Group B) or without rab bit serum (Group C) (P
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Objective To observe the protective effect of Xuefu Zhuyu Decoction (XZD) on vascular endothelial cells (VEC) injured by the serum of blood_stasis_syndrome ( BSS) rabbits. Methods The morphological features of VEC cultured with norma l rabbit serum (Group A), BSS rabbit serum(Group B), the serum of normal rabbit medicated with XZD(Group C) and the serum of BSS rabbit medicated with XZD(Group D) were observed respectively under light microscope and electron microscope. Results Under light microscope, VEC was shrinked, intercellular space widene d and cytoplasm contained dark granules in Group B. The change of intercellular space was not obvious in Group D. Under electron microscope, pinocytotic vesicle s increased, rough endoplasmic reticulum (RER) decreased and dilated, mitochondr ia became smaller and indistinct and only a small amount of microvilli appeared on cell membrane with top expanded and merged in VEC of Group B as compared with Group A and Group C. Less RER but no dilatation and fewer microvilli without to p merged were found in VEC of Group B. Conclusion The serum of BSS rabbits c an injury normal VEC cultured in vitro and XZD exerts a certain protective effe ct on VEC injured by the serum of BSS rabbits.
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Objective To explore methods for establishinga cellu lar injury model of blood stasis syndrome (BSS). Methods Two experiments were c arried out. In the first experiment,the injured vascular endothelial cell model of BSS was established by the culture of vascular endothelial cell, and in the seco nd experiment, the vascular endothelial cell injured by the serum of BSS rabbit was cultured. Results In the first experiment, pathological features and end ocrine dysfunction in the primary cultured endothelial cell were similar to the B SS rabbit model, but the above changes did not remain in the subculture. The above changes were also found in the second experiment and were easy to be repea ted. Conclusion The injured vascular endothelial cell model of BSS establis hed b y the above methods reflects or partially reflects the structure and function of BSS rabbit model and the patients with BSS, and can be used to study the pathol ogical mechanism of BSS and therapeutic effect of blood_circulation activating a nd blood_stasis removing herbs.
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Objective To explore the relationship between Qi_stagnation with blood stasi s, Qi_deficiency with blood stasis and platelet activation. Methods Expressi on levels of lysosomal integral membrane protein (CD?63), alpha_granu le membrane protein (CD?62?p) and thrombospondin (TSP)were the specific index es of platelet activation. Te chnique of monoclonal antibody analysis and flow cytometry were used to detect the expression levels of CD?63, CD?62?p and TSP. Fifty_eight cases of Qi_st agnation with blood stasis syndrome were allocated to Group A and 60 cases of Qi _deficiency with blood stasis syndrome to Group B, and 30 healthy volunteers ser ved as the control (Group C). Results Expression levels of CD63, CD62p an d TSP were higher in Group A than in Group B and Group C (P