It is now thought that atherosclerosis,although due to enhanced lipid deposition,is mainly the result of a series inflammatory process.Total saponins of Aralia elata(Miq) Seem(TASAES) from the Chinese traditional herb...It is now thought that atherosclerosis,although due to enhanced lipid deposition,is mainly the result of a series inflammatory process.Total saponins of Aralia elata(Miq) Seem(TASAES) from the Chinese traditional herb Longya Araliachinensis L.,a folk medicine used for treating various diseases,increasing energy and improving the body′s ability to prevent hypoxia in Asian countries has attracted widespread attention.However,the ability of TASAES on inflammation-triggered vascular endothelial cell injury,a key early event in the pathogenesis of atherosclerosis,and its potential mechanisms of this protection have never been demonstrated.The present study determined the anti-inflammatory and anti-apoptoticactivities and protective mechanisms of the total aralosides of Araliaelata(Miq) Seem(TASAES) ameliorate tumor necrosis factor-α(TNF-α)-induced human umbilical vein endothelial cells(HUVECs) injury.Our results indicate that TASAES pretreatment provided cytoprotective effects by suppressing TNF-α-induced HUVECs apoptosis,mitochondrial membrane depolarization,caspase-3 activation,and modulation of inflammatory factors(IL-6,MCP-1 and VCAM-1),meanwhile inhibiting NF-κB transcription.Furthermore,the effect was correlated with the activation of the PI3K/Akt signal pathway.Blocking Akt activation with the PI3K inhibitor LY294002 effectively reversed the protective effect of TASAES against TNF-α-induced cell apoptosis.Moreover,the PI3K inhibitor partially blocked the effects of TASAES on the increasing of Bcl-2 and Bcl-xl protein expression,and inactivation of Bax protein expression.In conclusion,the results showed that TASAES decreased the inflammation and apoptosis of HUVECs caused by TNF-α treatment,and PI3K played a crucial role in enhancing cell sur.vival during this process.展开更多
目的探讨可溶性肿瘤坏死因子样凋亡弱诱导剂(sTWEAK)与2型糖尿病(T2DM)患者动脉粥样硬化斑块形成的关系。方法选择2017年6-12月于海军军医大学(第二军医大学)第一附属医院内分泌科住院治疗的T2DM患者73例为研究对象。根据有无颈动脉和/...目的探讨可溶性肿瘤坏死因子样凋亡弱诱导剂(sTWEAK)与2型糖尿病(T2DM)患者动脉粥样硬化斑块形成的关系。方法选择2017年6-12月于海军军医大学(第二军医大学)第一附属医院内分泌科住院治疗的T2DM患者73例为研究对象。根据有无颈动脉和/或下肢动脉斑块将患者分为有斑块组(46例)和无斑块组(27例),比较两组患者的一般资料、血生物化学指标及血清sTWEAK水平。采用Spearman相关性分析评估血清sTWEAK水平与各临床参数的相关性。采用logistic回归分析评估动脉粥样硬化斑块形成的影响因素。结果有斑块组患者的年龄和血清sTWEAK水平均高于无斑块组[(55.87±10.65)岁vs(44.04±11.96)岁,P=0.001;79.53(26.87,113.03)pg/mL vs 47.70(18.62,78.15)pg/mL,P=0.018]。Spearman相关性分析显示,血清sTWEAK水平与患者年龄(r=0.247,P=0.035)、斑块数量(r=0.270,P=0.021)呈正相关。logistic回归分析显示,年龄是T2DM患者动脉粥样硬化斑块形成的独立危险因素(OR=1.091,95%CI 1.036~1.148,P=0.001),而血清sTWEAK水平并非独立危险因素(OR=1.012,95%CI 0.999~1.025,P=0.063)。结论伴有动脉粥样硬化斑块的T2DM患者有更高的血清sTWEAK水平,其血清sTWEAK水平的升高可能与年龄相关。展开更多
基金supported by National Natural Science Foundation of China(81374011) CAMS Innovation Fund for Medical Sciences(CIFMS)(2016-I2M-1-012)
文摘It is now thought that atherosclerosis,although due to enhanced lipid deposition,is mainly the result of a series inflammatory process.Total saponins of Aralia elata(Miq) Seem(TASAES) from the Chinese traditional herb Longya Araliachinensis L.,a folk medicine used for treating various diseases,increasing energy and improving the body′s ability to prevent hypoxia in Asian countries has attracted widespread attention.However,the ability of TASAES on inflammation-triggered vascular endothelial cell injury,a key early event in the pathogenesis of atherosclerosis,and its potential mechanisms of this protection have never been demonstrated.The present study determined the anti-inflammatory and anti-apoptoticactivities and protective mechanisms of the total aralosides of Araliaelata(Miq) Seem(TASAES) ameliorate tumor necrosis factor-α(TNF-α)-induced human umbilical vein endothelial cells(HUVECs) injury.Our results indicate that TASAES pretreatment provided cytoprotective effects by suppressing TNF-α-induced HUVECs apoptosis,mitochondrial membrane depolarization,caspase-3 activation,and modulation of inflammatory factors(IL-6,MCP-1 and VCAM-1),meanwhile inhibiting NF-κB transcription.Furthermore,the effect was correlated with the activation of the PI3K/Akt signal pathway.Blocking Akt activation with the PI3K inhibitor LY294002 effectively reversed the protective effect of TASAES against TNF-α-induced cell apoptosis.Moreover,the PI3K inhibitor partially blocked the effects of TASAES on the increasing of Bcl-2 and Bcl-xl protein expression,and inactivation of Bax protein expression.In conclusion,the results showed that TASAES decreased the inflammation and apoptosis of HUVECs caused by TNF-α treatment,and PI3K played a crucial role in enhancing cell sur.vival during this process.
文摘目的探讨可溶性肿瘤坏死因子样凋亡弱诱导剂(sTWEAK)与2型糖尿病(T2DM)患者动脉粥样硬化斑块形成的关系。方法选择2017年6-12月于海军军医大学(第二军医大学)第一附属医院内分泌科住院治疗的T2DM患者73例为研究对象。根据有无颈动脉和/或下肢动脉斑块将患者分为有斑块组(46例)和无斑块组(27例),比较两组患者的一般资料、血生物化学指标及血清sTWEAK水平。采用Spearman相关性分析评估血清sTWEAK水平与各临床参数的相关性。采用logistic回归分析评估动脉粥样硬化斑块形成的影响因素。结果有斑块组患者的年龄和血清sTWEAK水平均高于无斑块组[(55.87±10.65)岁vs(44.04±11.96)岁,P=0.001;79.53(26.87,113.03)pg/mL vs 47.70(18.62,78.15)pg/mL,P=0.018]。Spearman相关性分析显示,血清sTWEAK水平与患者年龄(r=0.247,P=0.035)、斑块数量(r=0.270,P=0.021)呈正相关。logistic回归分析显示,年龄是T2DM患者动脉粥样硬化斑块形成的独立危险因素(OR=1.091,95%CI 1.036~1.148,P=0.001),而血清sTWEAK水平并非独立危险因素(OR=1.012,95%CI 0.999~1.025,P=0.063)。结论伴有动脉粥样硬化斑块的T2DM患者有更高的血清sTWEAK水平,其血清sTWEAK水平的升高可能与年龄相关。
