Objective To investigate the clilic effects of the compound danshen diwan in menopause women with ST changes and angina.Methods56 menopause women with ST changes and angina were randomly divided into two groups,a controlled group(n=28)with base medicine treatment and a observed group(n=28)with the compound danshen diwan.The change of vasodilation endothelium functon and symptom relief were oberved before and after treatment in all patients.ResultsVasodilation endothelium functon were improved markedly in the observed group while the controlled group had no significantly changes;Meanwhile,the clinic relief rates of the observed group was markedly superor to that of controlled group.ConclusionThe compound danshen diwan would have a positive effect in menopause women with ST changes and angina.

Objective To investigate the role of Notch signaling in the progression of peritoneal fibrosis in a rat model induced by high glucose dialysate. Methods Male Sprague Dawley rats were subjected to daily peritoneal dialysis (PD) with a lactate-buffered solution containing 4.25% glucose. They were sacrificed at 2 and 4 weeks after PD. The parietal thickness was measured with Masson staining. The expression of TGF-β1, E-cadherin, α-SMA and collagen Ⅰ was examined by immunoblotting. The expression of Notch ligand Jagged-1 and the negative Notch signaling regulato--Numb was analyzed by both immunoblotting and RT-PCR. The expression of a Notch nuclear target gene Hcs-1 was examined by RT-PCR. Results Both HE and Masson trichrome staining revealed an increase in peritoneal thickness with a loss of mesothelial cells and a rich of collagen matrix deposition in the submesothelial zone was evident at 4 weeks after PD. Meanwhile, compared to healthy rats, the expression of TGF-β1, ct-SMA and collagen Ⅰ was significantly increased, but the expression of E-cadherin was decreased in peritoneum after PD treatment. It was difficult to detect the Jagged-1 and Hes-1 expression in normal peritoneum, but their expression was graduaUy increased after PD. In contrast, the expression level of Numb, a negative regulator of Notch signaling, was dramatically decreased after PD. Conclusions Notch signaling is activated during the process of PD-induced peritoneal fibrosis and the activation of Notch signaling is associated with the loss of negative regulation of Notch signaling via decreased expression of Numb. Inhibition of Notch signaling via overexpression of its negative regulators such as Numb may be a novel therapeutic approach for peritoneal fibrosis in PD patients.

OBJECTIVEAtherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells.

METHODSHuman umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS.

RESULTSExposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects.

CONCLUSIONLSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.

Apoptosis ; Cells, Cultured ; Flavonoids ; Human Umbilical Vein Endothelial Cells ; cytology ; metabolism ; Humans ; MAP Kinase Signaling System ; Nitric Oxide Synthase Type III ; metabolism ; Oxidative Stress ; Phosphorylation ; Reactive Oxygen Species ; metabolism ; Stress, Mechanical ; p38 Mitogen-Activated Protein Kinases ; metabolism

Objective Atherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS. Results Exposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects. Conclusion LSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.

Objective Atherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS. Results Exposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects. Conclusion LSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.