【目的】探讨高血压和高血压合并糖尿病患者血浆可溶性神经纤毛蛋白-1(NRP-1)的浓度与超氧化物歧化酶(SOD)活性的变化。【方法】本横断面研究共纳入88人,分为对照组(n=26)、高血压组(n=31)和高血压合并糖尿病组(n=31)。人群血浆NRP-1的浓度和SOD活性应用酶联免疫吸附法测定,同时检测血糖、糖化血红蛋白A1C(GHbA1c)和血脂的变化情况。【结果】单纯高血压组血清总胆固醇(TC)和体质量指数(BMI)显著高于对照组(P<0.05),而高血压合并糖尿病组血清TC、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、BMI和腰围(WC)均显著高于对照组(P<0.05)。单纯高血压组和高血压合并糖尿病组血浆NRP-1的浓度和SOD活性均低于对照组[NRP-1(ng/mL):6.8(6.0~8.3)、5.2(4.0~6.8)vs 8.9(7.7~10.0);SOD(U/mL):157.1±18.6、145.1±31.4 vs 168.4±23.1,P<0.05],而高血压合并糖尿病组与单纯高血压组比较血浆NRP-1的浓度和SOD活性更低,且差异也有统计学意义[NRP-1(ng/mL):5.2(4.0~6.8)vs 6.8(6.0~8.3);SOD(U/mL):145.1±31.4 vs 157.1±18.6,P<0.05]。对3组研究人群分别进行线性相关性分析发现,NRP-1与SOD之间均呈显著正相关(r=0.539,0.660,0.895,P<0.05)。【结论】单纯高血压和高血压合并糖尿病患者血浆NRP-1的浓度均降低,而且高血压合并糖尿病患者血浆NRP-1的浓度降低更明显,NRP-1的浓度下降可能与SOD活性的下降有关。
Objective:To investigate whether ginsenoside Rb1(Rb1)can protect human umbilical vein endothelial cells(HUVECs)against high glucose-induced apoptosis and examine the underlying mechanism.Methods:HUVECs were divided into 5 groups:control group(5.5 mmol/L glucose),high glucose(HG,40 mmol/L)treatment group,Rb1(50μmol/L)treatment group,Rb1 plus HG treatment group,and Rb1 and 3-(1 H-1,2,3-triazol-4-yl)pyridine(3-TYP,16μmol/L)plus HG treatment group.Cell viability was evaluated by cell counting kit-8 assay.Mitochondrial and intracellular reactive oxygen species were detected by Mito Sox Red mitochondrial superoxide indicator and dichloro-dihydro-fluorescein diacetate assay,respectively.Annexin V/propidium iodide staining and fluorescent dye staining were used to measure the apoptosis and the mitochondrial membrane potential of HUVECs,respectively.The protein expressions of apoptosis-related proteins[Bcl-2,Bax,cleaved caspase-3 and cytochrome c(Cyt-c)],mitochondrial biogenesis-related proteins[proliferator-activated receptor gamma coactivator 1-alpha,nuclear respiratory factor-1 and mitochondrial transcription factor A],acetylation levels of forkhead box O3 a and SOD2,and sirtuin-3(SIRT3)signalling pathway were measured by immunoblotting and immunoprecipitation.Results:Rb1 ameliorated survival in cells in which apoptosis was induced by high glucose(P<0.05 or P<0.01).Upon the addition of Rb1,mitochondrial and intracellular reactive oxygen species generation and malondialdehyde levels were decreased(P<0.01),while the activities of antioxidant enzymes were increased(P<0.05 or P<0.01).Rb1 preserved the mitochondrial membrane potential and reduced the release of Cyt-c from the mitochondria into the cytosol(P<0.01).In addition,Rb1 upregulated mitochondrial biogenesis-associated proteins(P<0.01).Notably,the cytoprotective effects of Rb1 were correlated with SIRT3 signalling pathway activation(P<0.01).The effect of Rb1 against high glucose-induced mitochondria-related apoptosis was restrained by 3-TYP(P<0.05 or P<0.01).Conclu
