Breviscapine inhibits high glucose-induced proliferation and migration of cultured vascular smooth muscle cells of rats via suppressing the ERK1/2 MAPK signaling pathway  

作　　者：Meng HE Zhi-min XUE Juan LI Bin-quan ZHOU 

机构地区：[1]The Department of Cardiology,Biomedical Research(Therapy)Center,Sir Run Run Shaw Hospital,College of Medicine,Zhejiang University,Hangzhou 310016,China

出　　处：《Acta Pharmacologica Sinica》2012年第5期606-614,共9页中国药理学报（英文版）

摘　　要：Aim： To investigate the influences of breviscapine, a flavonoid extracted from Erigeron breviscapus, on the proliferation and migration of vascular smooth muscle cells （VSMCs） cultured in a high glucose medium and the underlying mechanisms. Methods： VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats and cultured in vitro. Cell proliferation was evaluated using Counting Kit-8 cell viability assay. Cell migration was evaluated using transwell migration assay and in vitro scratch assay. The expression and activity of protein kinase C-132 （PKC-132）, extracellular signal-regulated kinase 1/2 （ERK1/2）, p38 mitogen-activated protein kinase （p38）, and JNK mitogen-activated protein kinase （JNK） were measured with Western blotting. Results： Exposure of VSMCs to a high glucose （25 mmol/L） medium significantly increased the proliferation and migration potential as compared to the control group. Pretreatment with breviscapine （65 pmol/L and 108 pmol/L） attenuated high glucose-enhanced pro- liferation and migration of VSMCs. Exposure of VSMCs to the high glucose medium activated both the PKC-132 and ERK1/2 MAPK, but not the p38 and JNK MAPK. Pretreatment with breviscapine （65 pmol/L and 108 pmol/L） blocked high glucose-induced increase of the ERK1/2 activity, but not that of the PKC-132 activity. Conclusion： Our study demonstrated that breviscapine ameliorates high glucose-induced proliferation and migration of VSMCs via inhibiting ERK1/2 MAPK signaling.Aim： To investigate the influences of breviscapine, a flavonoid extracted from Erigeron breviscapus, on the proliferation and migration of vascular smooth muscle cells （VSMCs） cultured in a high glucose medium and the underlying mechanisms. Methods： VSMCs were isolated from thoracic aortas of male Sprague-Dawley rats and cultured in vitro. Cell proliferation was evaluated using Counting Kit-8 cell viability assay. Cell migration was evaluated using transwell migration assay and in vitro scratch assay. The expression and activity of protein kinase C-132 （PKC-132）, extracellular signal-regulated kinase 1/2 （ERK1/2）, p38 mitogen-activated protein kinase （p38）, and JNK mitogen-activated protein kinase （JNK） were measured with Western blotting. Results： Exposure of VSMCs to a high glucose （25 mmol/L） medium significantly increased the proliferation and migration potential as compared to the control group. Pretreatment with breviscapine （65 pmol/L and 108 pmol/L） attenuated high glucose-enhanced pro- liferation and migration of VSMCs. Exposure of VSMCs to the high glucose medium activated both the PKC-132 and ERK1/2 MAPK, but not the p38 and JNK MAPK. Pretreatment with breviscapine （65 pmol/L and 108 pmol/L） blocked high glucose-induced increase of the ERK1/2 activity, but not that of the PKC-132 activity. Conclusion： Our study demonstrated that breviscapine ameliorates high glucose-induced proliferation and migration of VSMCs via inhibiting ERK1/2 MAPK signaling.

关 键 词：BREVISCAPINE vascular smooth muscle cells cell proliferation cell migration protein kinase C MAP kinase 

分 类 号：Q463[生物学—生理学] Q25