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机构地区:[1]广西医科大学生理学教研室,广西南宁530021 [2]广西医科大学肿瘤医院,广西南宁530027
出 处:《中国病理生理杂志》2007年第4期674-677,共4页Chinese Journal of Pathophysiology
基 金:广西自然科学基金资助项目(No.桂科自0229033)
摘 要:目的:探讨海带多糖L01抑制血小板活性与保护血管内皮细胞(VEC)的关系。方法:采用注射肾上腺素(Adr)法建立大鼠VEC损伤模型,滤过法测定大鼠血小板黏附性,火棉胶玻片法观察血小板表面聚集活性,酶联免疫吸附双抗体夹心(ELISA)法测定大鼠血浆血管性血友病因子(vWF)含量,免疫组化检测主动脉完整内皮长度(μm)。结果:模型组自造模第3 d起大鼠血小板聚集率、第4 d起血小板黏附率均分别高于生理盐水组(P<0.05,P<0.01),L01高剂量(50 mg/kg)、低剂量(10 mg/kg)组第4 d和第5 d大鼠的血小板黏附率和聚集率低于模型组(P<0.05,P<0.01);造模第4 d,模型组大鼠血浆vWF水平高于生理盐水组(P<0.05);L01高剂量组大鼠血浆vWF水平低于模型组(P<0.05);造模第5 d,模型组与生理盐水组比较、L01高、低剂量组与模型组比较,均呈现出同样的结果(P<0.05);造模第4 d和第5 d免疫组化检测主动脉完整内皮长度显示,模型组长度小于生理盐水组,L01高剂量、低剂量组长度明显大于模型组(P<0.05)。结论:L01抑制血小板活性的作用与保护VEC有关。AIM: To study the relationship between the effects of polysaccharide L01 extracted from laminaria japonica aresch on platelet activation and endothelial cells. METHODS: A rat model of endothelial injury was established via injecting adrenaline. The percentage of platelet adhesion was evaluated by filtration method, the activation of platelet aggregation was observed on a glass plate with collodion membrane, the content of vWF in rat plasma was measured by ELISA, the damaged degree of aortic vascular endothelial was evaluated by immunity histochemistry. RESULTS: The percentage of platelet adhesion and aggregation in model group were higher than those in NS group from the 3th and 4th day during the model made (P 〈0. 05, P 〈0. 01 ). The percentage in both L01 high - dose group (50 mg/kg) and low - dose group ( 10 mg/kg) at the 4th and 5th day was lower than that in model group (P 〈 0. 05, P 〈 0. 01 ). The content of vWF in rat plasma in model group was higher than that in NS group and in L01 high - dose group at 4th day ( P 〈 0. 05 ). The same results were presented by the comparison among model group and NS group, both L01 high - dose group and low - dose group at the 5 th ( P 〈 0. 05). The measure of intact endodermis lengths (μm) stained by immunohistochemistry demonstrated that the length in model group was shorter than that in NS group (P 〈0.05), whereas the length in L01 high - dose group and low - dose group was obviously longer than that in model group ( P 〈 0. 05 ) at the 4th and 5th day. CONCLUSION: The inhibitory effect of L01 on platelet activation may be related with its protective effect on vascular endothelial cells.
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