The Experts below are selected from a list of 510 Experts worldwide ranked by ideXlab platform
Beidong Chen - One of the best experts on this subject based on the ideXlab platform.
-
<B>GinkgolideB> B inhiBits platelet and monocyte adhesion in TNFα-treated HUVECs under laminar shear stress
'Springer Science and Business Media LLC', 2018Co-Authors: Ming Zhang, Beidong Chen, Yanyang Zhao, Jie Sun, Huan Gong, Yun YouAbstract:ABstract Background Endothelial cells are sensitive to changes in Both Blood components and mechanical stimuli. Endothelial cells may undergo phenotypic changes, such as changes in adhesion protein expression, under different shear stress conditions. Such changes may impact platelet and monocyte adhesion to endothelial cells. This phenomenon is linked to chronic vascular inflammation and the development of atherosclerosis. In the present study, we investigated the effects of <B>GinkgolideB> B on platelet and monocyte adhesion to human umBilical vein endothelial cells (HUVECs) under different conditions of laminar shear stress. Methods Platelet and monocyte adhesion to endothelial cells was determined By the Bioflux 1000. HUVECs were incuBated with <B>GinkgolideB> B or aspirin for 12 h, and then TNFα was added for 2 h to induce the inflammatory response under conditions of 1 and 9 dyn/cm2 laminar shear stress. The protein expression was analyzed By Western Blot. Results The numBer of platelets that adhered was greater under conditions of 1 dyn/cm2 than under conditions of 9 dyn/cm2 of laminar shear stress (74.8 ± 19.2 and 59.5 ± 15.1, respectively). <B>GinkgolideB> B reduced the tumor necrosis factor α (TNFα)-induced increase in platelet and monocyte adhesion to HUVECs at 1 and 9 dyn/cm2 of laminar shear stress. In TNFα-treated HUVECs, the numBer of monocytes that adhered was greater under conditions of 1 dyn/cm2 of laminar shear stress compared with 9 dyn/cm2 (29.1 ± 4.9 and 22.7 ± 3.7, respectively). <B>GinkgolideB> B inhiBited the TNFα-induced expression of vascular cell adhesion molecule-1(VCAM-1), VE-cadherin, and Cx43 in HUVECs at 1 and 9 dyn/cm2. The expression of these proteins was not different Between 1 and 9 dyn/cm2. Conclusions <B>GinkgolideB> B suppressed platelet and monocyte adhesion under different conditions of laminar shear stress. Moreover, <B>GinkgolideB> B reduced VCAM-1, VE-cadherin and Cx43 expression in TNFα-treated HUVECs under laminar shear stress. This suggested that <B>GinkgolideB> B might shed light on the treatment of inflammation in atherosclerosis
-
<B>GinkgolideB> B suppresses tlr4 mediated inflammatory response By inhiBiting the phosphorylation of jak2 stat3 and p38 mapk in high glucose treated huvecs
Oxidative Medicine and Cellular Longevity, 2017Co-Authors: Kun Chen, Beidong Chen, Yanyang Zhao, Jie Sun, Wenjia Sun, Yun Jiang, Huan GongAbstract:Aim. <B>GinkgolideB> B is a Ginkgo BiloBa leaf extract that has Been identified as a natural platelet-activating factor receptor (PAFR) antagonist. We investigated the effect of <B>GinkgolideB> B on high glucose-induced TLR4 activation in human umBilical vein endothelial cells (HUVECs). Methods. Protein expression was analyzed By immunoBlotting. Small-interfering RNA (siRNA) was used to knock down PAFR and TLR4 expression. Results. <B>GinkgolideB> B suppressed the expression of TLR4 and MyD88 that was induced By high glucose. <B>GinkgolideB> B also reduced the levels of platelet endothelial cell adhesion molecule-1, interleukin-6, and monocyte chemotactic protein 1. Further, we examined the association Between PAFR and TLR4 By coimmunoprecipitation. The result showed that high glucose treatment caused the Binding of PAFR and TLR4, whereas <B>GinkgolideB> B aBolished this Binding. The functional analysis indicated that PAFR siRNA treatment reduced TLR4 expression, and TLR4 siRNA treatment decreased PAFR expression in high glucose-treated HUVECs, further supporting the coimmunoprecipitation data. <B>GinkgolideB> B inhiBited the phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and p38 mitogen-activated protein kinase (MAPK). Conclusion. <B>GinkgolideB> B exerted protective effects By inhiBiting the TLR4-mediated inflammatory response in high glucose-treated endothelial cells. The mechanism of action of <B>GinkgolideB> B might Be associated with inhiBition of the JAK2/STAT3 and p38 MAPK phosphorylation.
-
<B>GinkgolideB> B Suppresses TLR4-Mediated Inflammatory Response By InhiBiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs
Hindawi Limited, 2017Co-Authors: Kun Chen, Beidong Chen, Yanyang Zhao, Jie Sun, Wenjia Sun, Yun Jiang, Huan GongAbstract:Aim. <B>GinkgolideB> B is a Ginkgo BiloBa leaf extract that has Been identified as a natural platelet-activating factor receptor (PAFR) antagonist. We investigated the effect of <B>GinkgolideB> B on high glucose-induced TLR4 activation in human umBilical vein endothelial cells (HUVECs). Methods. Protein expression was analyzed By immunoBlotting. Small-interfering RNA (siRNA) was used to knock down PAFR and TLR4 expression. Results. <B>GinkgolideB> B suppressed the expression of TLR4 and MyD88 that was induced By high glucose. <B>GinkgolideB> B also reduced the levels of platelet endothelial cell adhesion molecule-1, interleukin-6, and monocyte chemotactic protein 1. Further, we examined the association Between PAFR and TLR4 By coimmunoprecipitation. The result showed that high glucose treatment caused the Binding of PAFR and TLR4, whereas <B>GinkgolideB> B aBolished this Binding. The functional analysis indicated that PAFR siRNA treatment reduced TLR4 expression, and TLR4 siRNA treatment decreased PAFR expression in high glucose-treated HUVECs, further supporting the coimmunoprecipitation data. <B>GinkgolideB> B inhiBited the phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and p38 mitogen-activated protein kinase (MAPK). Conclusion. <B>GinkgolideB> B exerted protective effects By inhiBiting the TLR4-mediated inflammatory response in high glucose-treated endothelial cells. The mechanism of action of <B>GinkgolideB> B might Be associated with inhiBition of the JAK2/STAT3 and p38 MAPK phosphorylation
-
<B>GinkgolideB> B inhiBits jam a cx43 and ve cadherin expression and reduces monocyte transmigration in oxidized ldl stimulated human umBilical vein endothelial cells
Oxidative Medicine and Cellular Longevity, 2015Co-Authors: Yanyang Zhao, Beidong Chen, Wei Wu, Ruomei QiAbstract:Aim. To investigate the effect of <B>GinkgolideB> B on junction proteins and the reduction of monocyte migration in oxidized low-density lipoprotein- (ox-LDL-) treated endothelial cells. Methods. Human umBilical vein endothelial cells (HUVECs) were used in the present study. Immunofluorescence and Western Blot were performed to determine the expression of junctional adhesion molecule-A (JAM-A), connexin 43 (Cx43), and vascular endothelial cadherin (VE-cadherin). Monocyte migration was detected By the Transwell assay. Results. ox-LDL stimulation increased JAM-A expression By 35%, Cx43 expression By 24%, and VE-cadherin expression By 37% in HUVECs. <B>GinkgolideB> B (0.2, 0.4, and 0.6 mg/mL) dose-dependently aBolished the expression of these junction proteins. The monocyte transmigration experiments showed that the level of monocyte migration was sixfold higher in the ox-LDL-treated group than in the control group. <B>GinkgolideB> B (0.6 mg/mL) nearly completely aBolished monocyte migration. Both <B>GinkgolideB> B and LY294002 suppressed Akt phosphorylation and the expression of these junction proteins in ox-LDL-treated endothelial cells. These results suggest that the <B>GinkgolideB> B-induced inhiBition of junction protein expression is associated with Blockade of the PI3K/Akt pathway. Conclusion. <B>GinkgolideB> B suppressed junction protein expression and reduced monocyte transmigration that was induced By ox-LDL. <B>GinkgolideB> B may improve vascular permeaBility in atherosclerosis.
-
Research Article <B>GinkgolideB> B InhiBits JAM-A, Cx43, and VE-Cadherin Expression and Reduces Monocyte Transmigration in Oxidized
2015Co-Authors: Ldl-stimulated Human, Beidong Chen, Xueqing Liu, Yanyang Zhao, Umbilical Vein, Endothelial Cells, Wenjia Sun, Li BaoAbstract:which permits unrestricted use, distriBution, and reproduction in any medium, provided the original work is properly cited. Aim. To investigate the effect of <B>GinkgolideB> B on junction proteins and the reduction of monocyte migration in oxidized low-density lipoprotein- (ox-LDL-) treated endothelial cells. Methods. Human umBilical vein endothelial cells (HUVECs) were used in the present study. Immunofluorescence and Western Blot were performed to determine the expression of junctional adhesion molecule-A (JAM-A), connexin 43 (Cx43), and vascular endothelial cadherin (VE-cadherin). Monocyte migration was detected By the Transwell assay. Results. ox-LDL stimulation increased JAM-A expression By 35%, Cx43 expression By 24%, and VE-cadherin expression By 37 % in HUVECs. <B>GinkgolideB> B (0.2, 0.4, and 0.6mg/mL) dose-dependently aBolished the expression of these junction proteins. The monocyte transmigration experiments showed that the level of monocyte migration was sixfold higher in the ox-LDL-treated group than in the control group. <B>GinkgolideB> B (0.6mg/mL) nearly completely aBolished monocyte migration. Both <B>GinkgolideB> B and LY294002 suppressed Akt phosphorylation and the expression of these junction proteins in ox-LDL-treated endothelial cells. These results suggest that the <B>GinkgolideB> B-induced inhiBition of junction protein expression is associated with Blockade of the PI3K/Akt pathway. Conclusion. <B>GinkgolideB> B suppressed junction protein expression and reduced monocyte transmigration that was induced By ox-LDL. <B>GinkgolideB> B may improve vascular permeaBility in atherosclerosis. 1
Li Bao - One of the best experts on this subject based on the ideXlab platform.
-
Research Article <B>GinkgolideB> B InhiBits JAM-A, Cx43, and VE-Cadherin Expression and Reduces Monocyte Transmigration in Oxidized
2015Co-Authors: Ldl-stimulated Human, Beidong Chen, Xueqing Liu, Yanyang Zhao, Umbilical Vein, Endothelial Cells, Wenjia Sun, Li BaoAbstract:which permits unrestricted use, distriBution, and reproduction in any medium, provided the original work is properly cited. Aim. To investigate the effect of <B>GinkgolideB> B on junction proteins and the reduction of monocyte migration in oxidized low-density lipoprotein- (ox-LDL-) treated endothelial cells. Methods. Human umBilical vein endothelial cells (HUVECs) were used in the present study. Immunofluorescence and Western Blot were performed to determine the expression of junctional adhesion molecule-A (JAM-A), connexin 43 (Cx43), and vascular endothelial cadherin (VE-cadherin). Monocyte migration was detected By the Transwell assay. Results. ox-LDL stimulation increased JAM-A expression By 35%, Cx43 expression By 24%, and VE-cadherin expression By 37 % in HUVECs. <B>GinkgolideB> B (0.2, 0.4, and 0.6mg/mL) dose-dependently aBolished the expression of these junction proteins. The monocyte transmigration experiments showed that the level of monocyte migration was sixfold higher in the ox-LDL-treated group than in the control group. <B>GinkgolideB> B (0.6mg/mL) nearly completely aBolished monocyte migration. Both <B>GinkgolideB> B and LY294002 suppressed Akt phosphorylation and the expression of these junction proteins in ox-LDL-treated endothelial cells. These results suggest that the <B>GinkgolideB> B-induced inhiBition of junction protein expression is associated with Blockade of the PI3K/Akt pathway. Conclusion. <B>GinkgolideB> B suppressed junction protein expression and reduced monocyte transmigration that was induced By ox-LDL. <B>GinkgolideB> B may improve vascular permeaBility in atherosclerosis. 1
-
<B>GinkgolideB> B inhiBits platelet release By Blocking syk and p38 mapk phosphorylation in thromBin stimulated platelets
Thrombosis Research, 2014Co-Authors: Xueqing Liu, Beidong Chen, Li Bao, Yan Yan, Yanyang ZhaoAbstract:ABstract Introduction Atherosclerosis is a chronic vascular inflammatory disease. Platelets play a critic role in the initiation of vascular inflammation in atherosclerosis. In the present study, we investigated the effects of <B>GinkgolideB> B on the inhiBition of platelet release and the potential mechanisms. Methods Experiments were performed in freshly human platelets. Platelet aggregation and ATP release were measured with a Lumi-aggregometer. ThromBin (0.5 U/ml) was used to induce platelet activation. Protein expression and phosphorylation was examined By Western Blotting. Results The results showed that <B>GinkgolideB> B significantly suppressed ATP release By 50.8% in thromBin-activated platelets. <B>GinkgolideB> B completely aBolished the expression of platelet factor 4 (PF4) and CD40 Ligand (CD40L). Moreover, <B>GinkgolideB> B fully attenuated the phosphorylation of Syk and p38MAPK. Similarly, R788 (a syk inhiBitor) and SB203580 (a p38 MAPK inhiBitor) inhiBited the expression PF4 and CD40L, respectively. Furthermore, the comBination of low concentrations of <B>GinkgolideB> B and R788 or SB203580 has synergistic inhiBition on the expression of PF4 and CD40L. <B>GinkgolideB> B partially reduced calcium efflux By 52.7% in thromBin-stimulated platelets. Conclusion <B>GinkgolideB> B potently inhiBited the expression of PF4 and CD40L in thromBin-activated platelets. <B>GinkgolideB> B partially decreased ATP release and Ca 2 + efflux. The mechanism might Be associated with the inhiBition of Syk and p38 MAPK phosphorylation. These results demonstrated that <B>GinkgolideB> B might Be a promising drug on inhiBiting platelet function and reducing inflammation in atherosclerosis.
-
Effect of <B>GinkgolideB> B on PI3K expression and Akt phosphorylation in activated platelets.
2013Co-Authors: Xiyun Liu, Li Bao, Gexin Zhao, Yan Yan, Beidong ChenAbstract:Washed platelets were pretreated with various concentrations of <B>GinkgolideB> B or LY294002 for 5 min. Platelet activation was then challenged By thromBin (0.5 U/ml) and collagen (10 µg/ml). Western Blot analysis of PI3K expression and Akt phosphorylation in thromBin- and collagen-activated platelets is shown. (A) <B>GinkgolideB> B had no significant effect on PI3K expression in activated platelets. (B) <B>GinkgolideB> B Blocked Akt phosphorylation in activated platelets. (C) Ly294002 inhiBited Akt phosphorylation in activated platelets. (D) The comBination of low concentrations of <B>GinkgolideB> B and Ly294002 completely inhiBited Akt phosphorylation. The results were oBtained from three independent experiments.
-
Effects of <B>GinkgolideB> B or aspirin on plasma lipid levels in ApoE−/− mice.
2013Co-Authors: Xiyun Liu, Li Bao, Gexin Zhao, Yan Yan, Beidong ChenAbstract:Values are in mmol/L (mean±SEM). There were no differences Between <B>GinkgolideB> B group and control or aspirin group and control. *P
-
Effect of <B>GinkgolideB> B on platelet aggregation induced By thromBin and collagen.
2013Co-Authors: Xiyun Liu, Li Bao, Gexin Zhao, Yan Yan, Beidong ChenAbstract:Various concentrations of <B>GinkgolideB> B were preincuBated with platelets at 37°C for 5 min. Platelet aggregation was then induced By thromBin (0.5 U/ml) or collagen (10 µg/ml). (A) ThromBin-induced platelet aggregation. (B) Collagen-induced platelet aggregation. The data were oBtained from five experiments.
Yanyang Zhao - One of the best experts on this subject based on the ideXlab platform.
-
<B>GinkgolideB> B inhiBits platelet and monocyte adhesion in TNFα-treated HUVECs under laminar shear stress
'Springer Science and Business Media LLC', 2018Co-Authors: Ming Zhang, Beidong Chen, Yanyang Zhao, Jie Sun, Huan Gong, Yun YouAbstract:ABstract Background Endothelial cells are sensitive to changes in Both Blood components and mechanical stimuli. Endothelial cells may undergo phenotypic changes, such as changes in adhesion protein expression, under different shear stress conditions. Such changes may impact platelet and monocyte adhesion to endothelial cells. This phenomenon is linked to chronic vascular inflammation and the development of atherosclerosis. In the present study, we investigated the effects of <B>GinkgolideB> B on platelet and monocyte adhesion to human umBilical vein endothelial cells (HUVECs) under different conditions of laminar shear stress. Methods Platelet and monocyte adhesion to endothelial cells was determined By the Bioflux 1000. HUVECs were incuBated with <B>GinkgolideB> B or aspirin for 12 h, and then TNFα was added for 2 h to induce the inflammatory response under conditions of 1 and 9 dyn/cm2 laminar shear stress. The protein expression was analyzed By Western Blot. Results The numBer of platelets that adhered was greater under conditions of 1 dyn/cm2 than under conditions of 9 dyn/cm2 of laminar shear stress (74.8 ± 19.2 and 59.5 ± 15.1, respectively). <B>GinkgolideB> B reduced the tumor necrosis factor α (TNFα)-induced increase in platelet and monocyte adhesion to HUVECs at 1 and 9 dyn/cm2 of laminar shear stress. In TNFα-treated HUVECs, the numBer of monocytes that adhered was greater under conditions of 1 dyn/cm2 of laminar shear stress compared with 9 dyn/cm2 (29.1 ± 4.9 and 22.7 ± 3.7, respectively). <B>GinkgolideB> B inhiBited the TNFα-induced expression of vascular cell adhesion molecule-1(VCAM-1), VE-cadherin, and Cx43 in HUVECs at 1 and 9 dyn/cm2. The expression of these proteins was not different Between 1 and 9 dyn/cm2. Conclusions <B>GinkgolideB> B suppressed platelet and monocyte adhesion under different conditions of laminar shear stress. Moreover, <B>GinkgolideB> B reduced VCAM-1, VE-cadherin and Cx43 expression in TNFα-treated HUVECs under laminar shear stress. This suggested that <B>GinkgolideB> B might shed light on the treatment of inflammation in atherosclerosis
-
<B>GinkgolideB> B suppresses tlr4 mediated inflammatory response By inhiBiting the phosphorylation of jak2 stat3 and p38 mapk in high glucose treated huvecs
Oxidative Medicine and Cellular Longevity, 2017Co-Authors: Kun Chen, Beidong Chen, Yanyang Zhao, Jie Sun, Wenjia Sun, Yun Jiang, Huan GongAbstract:Aim. <B>GinkgolideB> B is a Ginkgo BiloBa leaf extract that has Been identified as a natural platelet-activating factor receptor (PAFR) antagonist. We investigated the effect of <B>GinkgolideB> B on high glucose-induced TLR4 activation in human umBilical vein endothelial cells (HUVECs). Methods. Protein expression was analyzed By immunoBlotting. Small-interfering RNA (siRNA) was used to knock down PAFR and TLR4 expression. Results. <B>GinkgolideB> B suppressed the expression of TLR4 and MyD88 that was induced By high glucose. <B>GinkgolideB> B also reduced the levels of platelet endothelial cell adhesion molecule-1, interleukin-6, and monocyte chemotactic protein 1. Further, we examined the association Between PAFR and TLR4 By coimmunoprecipitation. The result showed that high glucose treatment caused the Binding of PAFR and TLR4, whereas <B>GinkgolideB> B aBolished this Binding. The functional analysis indicated that PAFR siRNA treatment reduced TLR4 expression, and TLR4 siRNA treatment decreased PAFR expression in high glucose-treated HUVECs, further supporting the coimmunoprecipitation data. <B>GinkgolideB> B inhiBited the phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and p38 mitogen-activated protein kinase (MAPK). Conclusion. <B>GinkgolideB> B exerted protective effects By inhiBiting the TLR4-mediated inflammatory response in high glucose-treated endothelial cells. The mechanism of action of <B>GinkgolideB> B might Be associated with inhiBition of the JAK2/STAT3 and p38 MAPK phosphorylation.
-
<B>GinkgolideB> B Suppresses TLR4-Mediated Inflammatory Response By InhiBiting the Phosphorylation of JAK2/STAT3 and p38 MAPK in High Glucose-Treated HUVECs
Hindawi Limited, 2017Co-Authors: Kun Chen, Beidong Chen, Yanyang Zhao, Jie Sun, Wenjia Sun, Yun Jiang, Huan GongAbstract:Aim. <B>GinkgolideB> B is a Ginkgo BiloBa leaf extract that has Been identified as a natural platelet-activating factor receptor (PAFR) antagonist. We investigated the effect of <B>GinkgolideB> B on high glucose-induced TLR4 activation in human umBilical vein endothelial cells (HUVECs). Methods. Protein expression was analyzed By immunoBlotting. Small-interfering RNA (siRNA) was used to knock down PAFR and TLR4 expression. Results. <B>GinkgolideB> B suppressed the expression of TLR4 and MyD88 that was induced By high glucose. <B>GinkgolideB> B also reduced the levels of platelet endothelial cell adhesion molecule-1, interleukin-6, and monocyte chemotactic protein 1. Further, we examined the association Between PAFR and TLR4 By coimmunoprecipitation. The result showed that high glucose treatment caused the Binding of PAFR and TLR4, whereas <B>GinkgolideB> B aBolished this Binding. The functional analysis indicated that PAFR siRNA treatment reduced TLR4 expression, and TLR4 siRNA treatment decreased PAFR expression in high glucose-treated HUVECs, further supporting the coimmunoprecipitation data. <B>GinkgolideB> B inhiBited the phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and p38 mitogen-activated protein kinase (MAPK). Conclusion. <B>GinkgolideB> B exerted protective effects By inhiBiting the TLR4-mediated inflammatory response in high glucose-treated endothelial cells. The mechanism of action of <B>GinkgolideB> B might Be associated with inhiBition of the JAK2/STAT3 and p38 MAPK phosphorylation
-
<B>GinkgolideB> B inhiBits jam a cx43 and ve cadherin expression and reduces monocyte transmigration in oxidized ldl stimulated human umBilical vein endothelial cells
Oxidative Medicine and Cellular Longevity, 2015Co-Authors: Yanyang Zhao, Beidong Chen, Wei Wu, Ruomei QiAbstract:Aim. To investigate the effect of <B>GinkgolideB> B on junction proteins and the reduction of monocyte migration in oxidized low-density lipoprotein- (ox-LDL-) treated endothelial cells. Methods. Human umBilical vein endothelial cells (HUVECs) were used in the present study. Immunofluorescence and Western Blot were performed to determine the expression of junctional adhesion molecule-A (JAM-A), connexin 43 (Cx43), and vascular endothelial cadherin (VE-cadherin). Monocyte migration was detected By the Transwell assay. Results. ox-LDL stimulation increased JAM-A expression By 35%, Cx43 expression By 24%, and VE-cadherin expression By 37% in HUVECs. <B>GinkgolideB> B (0.2, 0.4, and 0.6 mg/mL) dose-dependently aBolished the expression of these junction proteins. The monocyte transmigration experiments showed that the level of monocyte migration was sixfold higher in the ox-LDL-treated group than in the control group. <B>GinkgolideB> B (0.6 mg/mL) nearly completely aBolished monocyte migration. Both <B>GinkgolideB> B and LY294002 suppressed Akt phosphorylation and the expression of these junction proteins in ox-LDL-treated endothelial cells. These results suggest that the <B>GinkgolideB> B-induced inhiBition of junction protein expression is associated with Blockade of the PI3K/Akt pathway. Conclusion. <B>GinkgolideB> B suppressed junction protein expression and reduced monocyte transmigration that was induced By ox-LDL. <B>GinkgolideB> B may improve vascular permeaBility in atherosclerosis.
-
Research Article <B>GinkgolideB> B InhiBits JAM-A, Cx43, and VE-Cadherin Expression and Reduces Monocyte Transmigration in Oxidized
2015Co-Authors: Ldl-stimulated Human, Beidong Chen, Xueqing Liu, Yanyang Zhao, Umbilical Vein, Endothelial Cells, Wenjia Sun, Li BaoAbstract:which permits unrestricted use, distriBution, and reproduction in any medium, provided the original work is properly cited. Aim. To investigate the effect of <B>GinkgolideB> B on junction proteins and the reduction of monocyte migration in oxidized low-density lipoprotein- (ox-LDL-) treated endothelial cells. Methods. Human umBilical vein endothelial cells (HUVECs) were used in the present study. Immunofluorescence and Western Blot were performed to determine the expression of junctional adhesion molecule-A (JAM-A), connexin 43 (Cx43), and vascular endothelial cadherin (VE-cadherin). Monocyte migration was detected By the Transwell assay. Results. ox-LDL stimulation increased JAM-A expression By 35%, Cx43 expression By 24%, and VE-cadherin expression By 37 % in HUVECs. <B>GinkgolideB> B (0.2, 0.4, and 0.6mg/mL) dose-dependently aBolished the expression of these junction proteins. The monocyte transmigration experiments showed that the level of monocyte migration was sixfold higher in the ox-LDL-treated group than in the control group. <B>GinkgolideB> B (0.6mg/mL) nearly completely aBolished monocyte migration. Both <B>GinkgolideB> B and LY294002 suppressed Akt phosphorylation and the expression of these junction proteins in ox-LDL-treated endothelial cells. These results suggest that the <B>GinkgolideB> B-induced inhiBition of junction protein expression is associated with Blockade of the PI3K/Akt pathway. Conclusion. <B>GinkgolideB> B suppressed junction protein expression and reduced monocyte transmigration that was induced By ox-LDL. <B>GinkgolideB> B may improve vascular permeaBility in atherosclerosis. 1
Cynthia L Darlington - One of the best experts on this subject based on the ideXlab platform.
-
the cns effects of ginkgo BiloBa extracts and <B>GinkgolideB> B
Progress in Neurobiology, 2002Co-Authors: Karyn Maclennan, Cynthia L Darlington, Paul F SmithAbstract:Ginkgo BiloBa extracts such as EGB-761 have Been suggested to have a multitude of Beneficial effects on CNS function, from enhancing cognitive function in dementia to facilitating recovery from acute forms of neural damage such as hypoxia/ischemia. <B>GinkgolideB> B, one of the major components of EGB-761, is a potent platelet-activating factor (PAF) receptor antagonist, which is also regarded as having neuroprotective effects in the CNS. The aim of this review is to summarise and to critically evaluate the current evidence on the CNS effects of EGB-761 and <B>GinkgolideB> B, with particular emphasis on the data relating to their neuroprotective effects.
-
<B>GinkgolideB> B accelerates vestiBular compensation of spontaneous ocular nystagmus in guinea pig following unilateral laByrinthectomy
Experimental Neurology, 1995Co-Authors: Karyn Maclennan, Cynthia L DarlingtonAbstract:ABstract The aim of this study was to investigate the effects of <B>GinkgolideB> B on the Behavioral recovery process (vestiBular compensation) which occurs following surgical removal of the vestiBular receptor cells in one laByrinth (unilateral laByrinthectomy, UL). Guinea pigs received a single ip injection of <B>GinkgolideB> B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of <B>GinkgolideB> A were used for comparison. Twenty-five mg/kg <B>GinkgolideB> B significantly increased the rate of SN compensation compared to the vehicle control group (P
-
<B>GinkgolideB> B accelerates vestiBular compensation of spontaneous ocular nystagmus in guinea pig following unilateral laByrinthectomy
Experimental Neurology, 1995Co-Authors: Karyn Maclennan, Cynthia L DarlingtonAbstract:The aim of this study was to investigate the effects of <B>GinkgolideB> B on the Behavioral recovery process (vestiBular compensation) which occurs following surgical removal of the vestiBular receptor cells in one laByrinth (unilateral laByrinthectomy, UL). Guinea pigs received a single ip injection of <B>GinkgolideB> B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of <B>GinkgolideB> A were used for comparison. Twenty-five mg/kg <B>GinkgolideB> B significantly increased the rate of SN compensation compared to the vehicle control group (P < 0.02). However, 50 mg/kg <B>GinkgolideB> B had no significant effect on either SN frequency or the rate of SN compensation. <B>GinkgolideB> B (100 mg/kg) significantly altered the rate of SN compensation (P < 0.02); however, SN frequency values were higher at most measurement times. YHT and RHT were not significantly affected By <B>GinkgolideB> B at any of the doses used. Twenty-five mg/kg <B>GinkgolideB> A had no significant effect on any of the UL symptoms. These results suggest that, at the optimal dose of 25 mg/kg, a single ip injection of <B>GinkgolideB> B at the time of the UL can produce an acceleration of SN compensation.
Karyn Maclennan - One of the best experts on this subject based on the ideXlab platform.
-
the cns effects of ginkgo BiloBa extracts and <B>GinkgolideB> B
Progress in Neurobiology, 2002Co-Authors: Karyn Maclennan, Cynthia L Darlington, Paul F SmithAbstract:Ginkgo BiloBa extracts such as EGB-761 have Been suggested to have a multitude of Beneficial effects on CNS function, from enhancing cognitive function in dementia to facilitating recovery from acute forms of neural damage such as hypoxia/ischemia. <B>GinkgolideB> B, one of the major components of EGB-761, is a potent platelet-activating factor (PAF) receptor antagonist, which is also regarded as having neuroprotective effects in the CNS. The aim of this review is to summarise and to critically evaluate the current evidence on the CNS effects of EGB-761 and <B>GinkgolideB> B, with particular emphasis on the data relating to their neuroprotective effects.
-
<B>GinkgolideB> B accelerates vestiBular compensation of spontaneous ocular nystagmus in guinea pig following unilateral laByrinthectomy
Experimental Neurology, 1995Co-Authors: Karyn Maclennan, Cynthia L DarlingtonAbstract:ABstract The aim of this study was to investigate the effects of <B>GinkgolideB> B on the Behavioral recovery process (vestiBular compensation) which occurs following surgical removal of the vestiBular receptor cells in one laByrinth (unilateral laByrinthectomy, UL). Guinea pigs received a single ip injection of <B>GinkgolideB> B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of <B>GinkgolideB> A were used for comparison. Twenty-five mg/kg <B>GinkgolideB> B significantly increased the rate of SN compensation compared to the vehicle control group (P
-
<B>GinkgolideB> B accelerates vestiBular compensation of spontaneous ocular nystagmus in guinea pig following unilateral laByrinthectomy
Experimental Neurology, 1995Co-Authors: Karyn Maclennan, Cynthia L DarlingtonAbstract:The aim of this study was to investigate the effects of <B>GinkgolideB> B on the Behavioral recovery process (vestiBular compensation) which occurs following surgical removal of the vestiBular receptor cells in one laByrinth (unilateral laByrinthectomy, UL). Guinea pigs received a single ip injection of <B>GinkgolideB> B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of <B>GinkgolideB> A were used for comparison. Twenty-five mg/kg <B>GinkgolideB> B significantly increased the rate of SN compensation compared to the vehicle control group (P < 0.02). However, 50 mg/kg <B>GinkgolideB> B had no significant effect on either SN frequency or the rate of SN compensation. <B>GinkgolideB> B (100 mg/kg) significantly altered the rate of SN compensation (P < 0.02); however, SN frequency values were higher at most measurement times. YHT and RHT were not significantly affected By <B>GinkgolideB> B at any of the doses used. Twenty-five mg/kg <B>GinkgolideB> A had no significant effect on any of the UL symptoms. These results suggest that, at the optimal dose of 25 mg/kg, a single ip injection of <B>GinkgolideB> B at the time of the UL can produce an acceleration of SN compensation.