Tanshinone IIA Represses c-fos、c-myc Expression of the Proliferating Vascular Smooth Muscle Cells Activated by Angiotensin II
Guangtian Yang
Abstract
Guangtian Yang
Abstract
Objective To study the effects of tanshinone ⅡA(TSN) to c-fos and c-myc of the proliferating vascular smooth muscle cell(VSMC) treated by angiotensin Ⅱ(AngⅡ). Methods A cell proliferating model of VSMC induced by angiotensin Ⅱ was established and then measured by MTT colorimetric assay.The effects of TSN on cell cycle of VSMC was detected by flow cytometry and on c-fos and c-myc gene expression by immunocytochemical staining(A value). Results The rat aortic smooth muscle cells were cultured in vitro successfully.The proportion of VSMC G0/G1 period was ascended by TSN(P0.01) and the proportion of VSMC S period was descended(P0.01).Cell proliferation activity and the expression levels of c-fos and c-myc were increased significantly in proliferating VSMC induced by AngⅡ(P0.01).While treated with TSN,the indexes were obviously reduced in a dose-dependent manner(0.001,0.010,0.100 mg·L-1)(P0.05,P0.01). Conclusion AngⅡ significantly stimulated the proliferation of VSMC.The VSMC proliferation induced by AngⅡ can be inhibited by TSN in dose-dependent manner and the mechanism may be that TSN decreases the expression levels of c-fos and c-myc.
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Objective To study the effects of tanshinone ⅡA(TSN) to c-fos and c-myc of the proliferating vascular smooth muscle cell(VSMC) treated by angiotensin Ⅱ(AngⅡ). Methods A cell proliferating model of VSMC induced by angiotensin Ⅱ was established and then measured by MTT colorimetric assay.The effects of TSN on cell cycle of VSMC was detected by flow cytometry and on c-fos and c-myc gene expression by immunocytochemical staining(A value). Results The rat aortic smooth muscle cells were cultured in vitro successfully.The proportion of VSMC G0/G1 period was ascended by TSN(P0.01) and the proportion of VSMC S period was descended(P0.01).Cell proliferation activity and the expression levels of c-fos and c-myc were increased significantly in proliferating VSMC induced by AngⅡ(P0.01).While treated with TSN,the indexes were obviously reduced in a dose-dependent manner(0.001,0.010,0.100 mg·L-1)(P0.05,P0.01). Conclusion AngⅡ significantly stimulated the proliferation of VSMC.The VSMC proliferation induced by AngⅡ can be inhibited by TSN in dose-dependent manner and the mechanism may be that TSN decreases the expression levels of c-fos and c-myc.
Key concepts: Vascular smooth muscle, Angiotensin II, Flow cytometry, Cell growth, c-Fos, Cell, In vitro, Chemistry