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 RESEARCH ARTICLE
Year : 2013  |  Volume : 45  |  Issue : 5  |  Page : 483-489

Panaxquin quefolium diolsaponins dose-dependently inhibits the proliferation of vascular smooth muscle cells by downregulating proto-oncogene expression


1 Department of Emergency, The Bethune First Hospital of Jilin University, Changchun 130021, China
2 Department of Gastroenterology, The Bethune First Hospital of Jilin University, Changchun 130021, China
3 Department of Cardiovascular Medicine, The Bethune First Hospital of Jilin University, Changchun 130021, China

Correspondence Address:
Xuezhong Zhao
Department of Cardiovascular Medicine, The Bethune First Hospital of Jilin University, Changchun 130021
China
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Source of Support: The Scientific and Technological Project of Traditional Chinese Medicine from Jilin Province Administration of Traditional Chinese Medicine (Grant No. 2004-096), People's Republic of China, Conflict of Interest: None


DOI: 10.4103/0253-7613.117772

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Objectives: Panax quinquefolium saponins (PQS) potentially prevent atherosclerosis in vivo. The proliferation of vascular smooth muscle cells (VSMCs) plays an important role in coronary heart disease and restenosis after percutaneous coronary intervention. Here, we investigated the potential effect of Panax quinquefolium diolsaponins (PQDS), a subtype of PQS, on angiotensin II (AngII)-induced VSMC proliferation. Materials and Methods: Isolated rat VSMCs were identified by immunocytochemical analysis. Cell proliferation was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cell cycle and proliferation index were analyzed using flow cytometry. The messenger ribonucleic acid (mRNA) expression of proto-oncogenes was evaluated using reverse transcription polymerase chain reaction. Results: Over 98% of cultured VSMCs were immunopositive for anti-α-smooth muscle actin. AngII promoted cell proliferation, whereas PQDS significantly suppressed VSMC growth in a dose-dependent manner. Moreover, PQDS suppressed AngII-induced proliferation of VSMCs by arresting the Gap 0/Gap 1 phase. Down-regulated mRNA expressions of proto-oncogenes occurred after PQDS application. Conclusions: Our study demonstrates that PQDS may reduce AngII-stimulated VSMC proliferation by suppressing the expression of proto-oncogenes. These results may provide insights for the development of novel traditional Chinese medicines to prevent atherosclerosis.






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