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Protective effects of cariporide on endothelial dysfunction induced by high glucose

Protective effects of cariporide on endothelial dysfunction induced by high glucose

作     者:Shuang-xi WANG Xiao-ming XIONG Tao SONG Li-ying LIU~2 Department of Pharmacology,Pharmaceutical College,Central South Universi~ Changsha 410078,China 

作者机构:Department of Pharmacology Pharmaceutical College Central South University Changsha China 

出 版 物:《Acta Pharmacologica Sinica》 (中国药理学报(英文版))

年 卷 期:2005年第26卷第3期

页      面:329-333页

核心收录:

学科分类:1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基  金:Project supported by the National Natural Science Foundation of China (№ 39770857) 

主  题:sodium-hydrogen antiporter endothelium glucose nitric oxide malondialdehyde superoxide dismutase 

摘      要:Aim:To explore the effects of cariporide,a selective sodium-hydrogen antiporterinhibitor,on endothelial dysfunction induced by high ***:Acetyl-choline (ACh)-induced endothelium-dependent relaxation (EDR),sodium nitro-prusside (SNP)-induced endothelium-independent relaxation and biochemical pa-rameters including malondialdehyde (MDA),superoxide dismutase (SOD),andnitric oxide (NO) were measured in rat isolated ***:A 6-h incubationof aortic rings with high glucose (44 mmol/L) resulted in a significant inhibitionof EDR,but had no effects on endothelium-independent *** the 6-hincubation of aortic rings in the co-presence of cariporide (0.01,0.1,and 1 μmol/L)with high glucose,cariporide prevented the inhibition of EDR caused by highglucose in concentration-dependent ***,high glucose decreasedSOD activity and contents of NO,and increased MDA concentration in *** (1 μmol/L) significantly resisted the decrease of NO contentand SOD activity,and elevation of MDA concentration caused by high glucose inaortic *** (44 mmol/L) or cariporide (1 μmol/L) alone had no ef-fect on EDR,endothelium-independent relaxation and biochemical ***:Cariporide significantly prevented endothelial dysfunction inducedby high *** mechanisms of endothelial dysfunction induced by highglucose may involve the activation of sodium-hydrogen antiporter and the gen-eration of oxygen-free radicals,but it is not related to the change of osmolarity.

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