氨基胍抑制高果糖诱导脑血管平滑肌细胞增殖的作用和机制  

Study on the Inhibition of Aminoguanidine on High-fructose Induced Proliferation of Smooth Muscle Cells of Basilar Artery and the Underlying Mechanisms

作　　者：郑凌云 董艳芬[1] 梁艳玲[1] 

机构地区：[1]广东药学院基础学院生理学系,广东广州510006

出　　处：《实用预防医学》2012年第7期1070-1072,共3页Practical Preventive Medicine

摘　　要：目的研究氨基胍对高果糖诱导的大鼠脑基底动脉血管平滑肌细胞增殖的影响和机制。方法原代培养大鼠脑基底动脉血管平滑肌细胞,用CCK8法测定不同浓度(50、100μmo/lL)氨基胍对15和30 mmo/lL果糖预诱导的血管平滑肌细胞增殖的影响。western blotting方法检测高果糖刺激后AKT以及JNK激酶表达的变化;以及检测不同浓度氨基胍预处理后对上述指标的影响。结果高果糖(30 mmo/lL)显著促进大鼠脑基底动脉血管平滑肌细胞增殖(0.768±0.032比0.374±0.054,P<0.01),在给予不同浓度(50、100μmo/lL)氨基胍后,平滑肌细胞增殖明显下降(0.584±0.063和0.387±0.031比0.768±0.032,P<0.01)。高果糖还明显刺激AKT以及JNK蛋白的表达,而给予氨基胍后可有效抑制上述蛋白表达。结论高果糖可诱导脑基底动脉血管平滑肌细胞增殖,而氨基胍可能通过抑制MAPK以及PI3K信号途径改善高果糖对平滑肌的增殖作用。Objective To investigate the effects of aminoguanidine（AG） on high-fructose induced proliferation of vascular smooth muscle cells of basilar artery（BASMCs） and to explore the underlying mechanisms.Methods BASMCs were isolated from male Sprague-Dawley rats and subject to primary culture.The proliferation index of BASMCs induced by D-fructose（15 and 30mmol/L） was investigated by CCK8 assays,and the expressions of AKT and JNK in BASMCs were detected by Western blotting.The inhibition of AG（50,100μmol/L） on the proliferation of BASMCs and AKT and JNK expressions were determined.Results High fructose（30mmol/L） markedly stimulated the proliferation of BASMCs（0.768±0.032 vs 0.374±0.054,P0.01）.Pretreatment with AG（50,100μmol/L） significantly inhibited BASMCs proliferation（0.584±0.063 and 0.387±0.031 vs 0.768±0.032,P0.01）.AG also inhibited the expressions of AKT and JNK stimulated by high fructose.Conclusions Aminoguanidine can inhibit the proliferation of BASMCs induced by high fructose,which may be attributed to the suppression of MAPK and PI3K signaling pathways.

关 键 词：氨基胍 D-果糖 脑基底动脉 血管平滑肌细胞 

分 类 号：R-332[医药卫生]