Objective To investigate lipopolysaccharide （LPS） induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B （BN52021）. Methods Thirty Sprague-Dawley rats were randomly divided into 3 gr...Objective To investigate lipopolysaccharide （LPS） induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B （BN52021）. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups （n = 10 for each group）： Control group, Model group and Treatment group （treated with BN52021）. LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method. Results The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.展开更多
Blood samples were harvested from the antecubital vein of 20 fasting patients with acute cerebral infarction at 1, 7 and 15 days after onset to prepare blood platelet suspension. Fasting antecubital vein blood was col...Blood samples were harvested from the antecubital vein of 20 fasting patients with acute cerebral infarction at 1, 7 and 15 days after onset to prepare blood platelet suspension. Fasting antecubital vein blood was collected from an additional 20 normal adults as controls. Under transmission elec- tron microscope, platelet Golgi tubules and vesicles became significantly thickened, enlarged, and irregular after acute cerebral infarction. Alpha granules in platelets significantly reduced in number, especially 1 day after cerebral infarction. Under immunoelectron microscopy, a few alpha granules aggregated around Golgi tubules and vesicles after infarction. These results suggested that platelet Golgi apparatus displayed significant morphological changes, which were possibly associated with enhanced synthetic and secretory functions of activated platelets after acute cerebral infarction. This study used Golgi apparatus blocking agent Brefeldin A to block Golgi apparatus in an aim to study the effects of Golgi apparatus on CD40L expression on the surface of activated platelets. Flow cytometry revealed that CD40L expression on activated platelet surfaces decreased significantly when Golgi apparatus was blocked, which indicated that Golgi apparatus participated in the syn- thesis and transport of CD40L to the platelet surface.展开更多
Objective To discuss the possible role of platelets in Binswanger’s disease by studying the changes of organelles and membrane glycoprotein in platelets Methods The organelles (dense bodies, alpha granules, and mi...Objective To discuss the possible role of platelets in Binswanger’s disease by studying the changes of organelles and membrane glycoprotein in platelets Methods The organelles (dense bodies, alpha granules, and mitochondria) within platelets were measured with transmission electron microscopy in 25 patients with Binswanger’s disease and matched controls, while alpha granule membrane glycoprotein CD62 and lysosomal integral membrane glycoprotein CD63 on platelet membrane were analyzed by flow cytometry Results The percentage of CD62 positive platelets was 3 6%±2 1% and 5 7%±2 4% in controls and in patients, respectively ( P <0 01) The percentage of CD63 expression platelets was 3 1%±2 2% and 3 2%±2 3% in controls and patients, respectively ( P >0 05) When compared with controls, platelets of patients contained fewer alpha granules ( P <0 01), and had no changes in dense bodies and mitochondria ( P >0 05) CD62 levels were different among patients with regarding to the degree of white matter low attenuation Conclusion There is selective degranuation of platelets in patients with Binswanger’s disease and the abnormalities of platelet secretion may play a role in the pathophysiology of this illness展开更多
文摘Objective To investigate lipopolysaccharide （LPS） induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B （BN52021）. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups （n = 10 for each group）： Control group, Model group and Treatment group （treated with BN52021）. LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method. Results The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly. Conclusion LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.
基金supported by grants from the National Natural Science Foundation of China, No.81171239/H0914Frontier Research Key Project,Central South University in China (2010-2011), No.2177-721500065the Education Expenditure of Hunan Provincial Finance Department in China, No.2010163
文摘Blood samples were harvested from the antecubital vein of 20 fasting patients with acute cerebral infarction at 1, 7 and 15 days after onset to prepare blood platelet suspension. Fasting antecubital vein blood was collected from an additional 20 normal adults as controls. Under transmission elec- tron microscope, platelet Golgi tubules and vesicles became significantly thickened, enlarged, and irregular after acute cerebral infarction. Alpha granules in platelets significantly reduced in number, especially 1 day after cerebral infarction. Under immunoelectron microscopy, a few alpha granules aggregated around Golgi tubules and vesicles after infarction. These results suggested that platelet Golgi apparatus displayed significant morphological changes, which were possibly associated with enhanced synthetic and secretory functions of activated platelets after acute cerebral infarction. This study used Golgi apparatus blocking agent Brefeldin A to block Golgi apparatus in an aim to study the effects of Golgi apparatus on CD40L expression on the surface of activated platelets. Flow cytometry revealed that CD40L expression on activated platelet surfaces decreased significantly when Golgi apparatus was blocked, which indicated that Golgi apparatus participated in the syn- thesis and transport of CD40L to the platelet surface.
文摘Objective To discuss the possible role of platelets in Binswanger’s disease by studying the changes of organelles and membrane glycoprotein in platelets Methods The organelles (dense bodies, alpha granules, and mitochondria) within platelets were measured with transmission electron microscopy in 25 patients with Binswanger’s disease and matched controls, while alpha granule membrane glycoprotein CD62 and lysosomal integral membrane glycoprotein CD63 on platelet membrane were analyzed by flow cytometry Results The percentage of CD62 positive platelets was 3 6%±2 1% and 5 7%±2 4% in controls and in patients, respectively ( P <0 01) The percentage of CD63 expression platelets was 3 1%±2 2% and 3 2%±2 3% in controls and patients, respectively ( P >0 05) When compared with controls, platelets of patients contained fewer alpha granules ( P <0 01), and had no changes in dense bodies and mitochondria ( P >0 05) CD62 levels were different among patients with regarding to the degree of white matter low attenuation Conclusion There is selective degranuation of platelets in patients with Binswanger’s disease and the abnormalities of platelet secretion may play a role in the pathophysiology of this illness
