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Objective To investigate the effect of Rhodiola on levels of inflammatory mediators and vascular endothelial function in rats with cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH).Methods Forty adult male SD rats were randomly divided into the sham operation group, model group, low-dose Rhodiola group, and high-dose Rhodiola group, with 10 rats in each group.Except for the sham operation group, rat models of CVS after SAH were established by cisterna magna twice method.1-5 d after modeling, the model group were treated with intraperitoneal injection of normal saline.The low-dose and high-dose Rhodiola groups were injected with 5mg/kg and 10mg/kg of Rhodiola respectively.5 days later, docking was performed and blood was collected to determine the levels of serum endothelin-1 (ET-1), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and cyclic guanosine monophosphate (cGMP).Then the rats were killed, and HE staining was performed to measure the diameter of basilar artery.The expression levels of basilar artery interleukin-6 (IL-6) mRNA, interleukin-1 β (IL-1 β) mRNA, vascular endothelial growth factor (VEGF) mRNA, endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) were determined by real-time fluorescence quantitative polymerase chain reaction (RT-q-PCR).Results (1) The diameters of basilar arteries showed model group ＜ low-dose and high-dose groups ＜ the sham operation group (P ＜ 0.05).(2) The levels of ET-1, IL-6, TNF-α, IL-6 mR-NA, IL-1β mRNA and iNOS mRNA showed model group ＞ low-dose and high-dose Rhodiola groups ＞ the sham operation group while levels of cGMP, VEGF mRNA and eNOS mRNA showed model group ＜ low dose and high-dose Rhodiola groups ＜ the sham operation group (P ＜ 0.05).Conclusions Rhodiola can reduce the expressions of inflammatory reactions, improve the vascular endothelial function, and promote the expressions of vascular endothelial growth factor in rats with CVS after SAH.
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Objective To investigate sitagliptin and repaglinide could ameliorate endothelial function in newly diagnosed type 2 diabetes patients and to explore its mechanism.Methods A total of 92 newly diagnosed type 2 diabetes patients with glycated hemoglobin A1c (HbA1c) from 6.5％ to 8.5％ was randomly assigned to sitagliptin group(n =46) receiving sitagliptin,and repaglinide group (n =46) receiving repaglinide for 12 weeks.The effect of sitagliptin on vascular endothelial function was measured with endothelium-dependent flow-mediated vasodilation (FMD).FMD,level of serum nitric oxide (NO),plasminogen activator inhibitor-1 (PAI-1) and biochemical variables in the two groups were measured at baseline and 12 weeks after treatment.Results Fasting blood glucose (FBG),postprandial blood glucose (PBG),and HbA1c decreased significantly both in sitagliptin and repaglinide groups after treatment,but the descent more significantly in the repaglinide group than those in the sitagliptin group (P ＜ 0.05).FMD,NO,and homeostasis model assessmentβ (HOMA-[β) were increased,and PAI-1 and homeostasis model assessment-insulin resistance (HOMR-IR) decreased in both two groups of patients (P ＜ 0.05).FMD,NO,and PAI-1 improved more significantly in sitagliptin groups (P ＜ 0.05).With FMD as dependent variables,multiple linear regression analysis showed that NO was a major protection factors of endothelial function,and PAI-1 and mean artery pressure (MAP) were major injury factors of endothelial function.Furthermore,with /FMD as the dependent variable,FMD as the dependent variable,and body mass index (BMI),MAP,HbA1c,HOMA-IR,triglycerides (TG),NO,and PAI-1 as a covariate-linear analysis of covariance showed that improved FMD with NO and PAI-1 were still relevant after treatment with sitagliptin.Conclusions Sitagliptin could improve vascular endothelial function evaluated by FMD better than repaglinide in newly diagnosed type 2 diabetes,the partial mechanism was related to the increase of NO level and the decrease of PAI-1 level,and the effect may be independent of the hypoglycemic effect.
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Objective To investigate sitagliptin and repaglinide could ameliorate endothelial function in newly diagnosed type 2 diabetes patients and to explore its mechanism.Methods A total of 92 newly diagnosed type 2 diabetes patients with glycated hemoglobin A1c (HbA1c) from 6.5％ to 8.5％ was randomly assigned to sitagliptin group(n =46) receiving sitagliptin,and repaglinide group (n =46) receiving repaglinide for 12 weeks.The effect of sitagliptin on vascular endothelial function was measured with endothelium-dependent flow-mediated vasodilation (FMD).FMD,level of serum nitric oxide (NO),plasminogen activator inhibitor-1 (PAI-1) and biochemical variables in the two groups were measured at baseline and 12 weeks after treatment.Results Fasting blood glucose (FBG),postprandial blood glucose (PBG),and HbA1c decreased significantly both in sitagliptin and repaglinide groups after treatment,but the descent more significantly in the repaglinide group than those in the sitagliptin group (P ＜ 0.05).FMD,NO,and homeostasis model assessmentβ (HOMA-[β) were increased,and PAI-1 and homeostasis model assessment-insulin resistance (HOMR-IR) decreased in both two groups of patients (P ＜ 0.05).FMD,NO,and PAI-1 improved more significantly in sitagliptin groups (P ＜ 0.05).With FMD as dependent variables,multiple linear regression analysis showed that NO was a major protection factors of endothelial function,and PAI-1 and mean artery pressure (MAP) were major injury factors of endothelial function.Furthermore,with /FMD as the dependent variable,FMD as the dependent variable,and body mass index (BMI),MAP,HbA1c,HOMA-IR,triglycerides (TG),NO,and PAI-1 as a covariate-linear analysis of covariance showed that improved FMD with NO and PAI-1 were still relevant after treatment with sitagliptin.Conclusions Sitagliptin could improve vascular endothelial function evaluated by FMD better than repaglinide in newly diagnosed type 2 diabetes,the partial mechanism was related to the increase of NO level and the decrease of PAI-1 level,and the effect may be independent of the hypoglycemic effect.
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Objective .To prove aristolochic (AA) caused vascular endothelial cells (VEC) injury via intracellular calcium overloa-ding and investigate the mechanism of calcium dobesilate antagonism. Methods Human umbilical vein endothelial cells (HUVEC) were cultured in vitro, and randomly divided into three groups: Control group, AA group, intervention group. Microscope and transmission elec-tron microscopy were used to observe changes of cell morphology and ultrastructure. ELISA method were applied to determine thrombomedu-lin (TM) in cell culture supernatant, fluorescent indicator FLuo-3/AM and intracellular calcium concentration ([Ca2+]. Results TM val-ue and average [Ca2+] i of AA group were significantly higher than that of control group (P < 0.05). Compared with the AA group, when the concentration of calcium dobesilate was 25 μM or 50 μM, TM value and average [Caz +] significantly decreased in intervention group (P < 0.05). Compared with control group, endoplasmic reticulum was pool expansion shaped, and mitochondrial cristae was absent in AA group cells. Endoplasmic reticulum and mitochondria patterns in the intervention group cells showed some improvement, compared with AA group. Conclusion AA induced VEC calcium overloading, 'I'M secretion and injury of endothelial ceils, endoplasmic reticulum and mito-chondria destruction. Dabesilate calcium could protect endoplasmic reticulum and mitochondria and reduce AA induced VEC calcium over-loading, and these could protect VEC.
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Objective To investigate the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell from apoptosis in cerebral ischemia-reperfusion injury. Methods Healthy, clean SD rats were randomly divided into 4 groups: Sham opera-tion group (SOG), cerebral ischemia reperfusion injury group (IRG), cerebral ischemia preconditioning group (IPG) and Chinese tradi-tional medicine mixture preconditioning group (CPG). Furthermore, IRG, IPG and NPC were divided into 4 sub-groups: 1 d, 7d, 14d, 21d subgroup, according to the different time point since ischemia-reperfusion took place. And in CPG, Naotai formula extract was used. Cere-bral vascular endothelial cells of rats were removed and Hoechst 33258 staining and the DNA gradient bands were used to detect the apoptosis of these cells. Then the influence of Naotai formula extract on caspase-3, 8 and 9 activation, and Bid lysis was examined by Western-blot, and the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell were investigated from apoptosis signal pathway. Result Naotai formula extract can inhibit the apoptosis of endothelial cells in ischemia-reperfusion injury, and it also can inhibit the activation of caspase-3, 8 and 9, thus inhibit the lysis of Bid into tBid. Conclusion Naomi formula extract inhibit the apoptosis of endo-thelial ceils in ischemia-reperfusion injury via apoptosis signal pathway.