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Objective:To investigate the effect of 2,3,4’,5-tetrahydroxystilbene-2-0- p-D-glucoside(TSG),an active component extracted from the root of Polygonum multiflorum,on angiotensin Ⅱ(Ang Ⅱ)-induced proliferation of cultured rat vascular smooth muscle cells(VSMCs) and to identify the potential mechanism.Methods:Cell proliferation and cell cycle were determined by cell counting,5-bromo-2’-deoxyuridine incorporation assay,proliferating cell nuclear antigen protein expression and flow cytometry.Levels of phosphorylated extracellular signal-regulated kinase 1/2(ERK1/2),mitogenic extracellular kinase 1/2(MEK1/2) and Src in VSMCs were measured by Western blot.The expression of c-fos,c-jun and c-myc mRNA were measured by reverse transcription polymerase chain reaction(RT-PCR).Intracellular reactive oxygen species(ROS) was measured by fluorescence assay.Results:TSG significantly inhibited Ang Ⅱ-induced VSMCs proliferation and arrested cells in the G_1/S checkpoint(P<0.05 or P<0.01).TSG decreased the levels of phosphorylated ERK1/2,MEK1/2 and Src in VSMCs(P<0.05 or P<0.01).TSG also suppressed c-fos,c-jun and c-myc mRNA expression(P<0.05 or P<0.01).In addition,the intracellular ROS was reduced by TSG(P<0.01).Conclusions:TSG inhibited Ang Ⅱ-induced VSMCs proliferation.Its antiproliferative effect might be associated with down-regulation of intracellular ROS,followed by the suppression of the Src-MEK1/2-ERK1/2 signal pathway,and hence,blocking cell cycle progression.
Objective: To investigate the effect of 2,3,4 ’, 5-tetrahydroxystilbene-2-0-pD-glucoside (TSG), an active component extracted from the root of Polygonum multiflorum, on angiotensin II (Ang II) -induced proliferation of cultured rat vascular smooth muscle cells (VSMCs) and to identify the potential mechanism. Methods: Cell proliferation and cell cycle were determined by cell counting, 5-bromo-2’-deoxyuridine incorporation assay, proliferating cell nuclear antigen protein expression and flow cytometry .Levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1 / 2), mitogenic extracellular kinase 1/2 (MEK1 / 2) and Src in VSMCs were measured by Western blot.The expression of c-fos, c-jun and Results: TSG significantly inhibited Ang II-induced VSMC proliferation and arrested cells in the G_1 / S (c-myc mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR) checkpoint (P <0.05 or P <0.01) .TSG decrea The levels of phosphorylated ERK1 / 2, MEK1 / 2 and Src in VSMCs (P <0.05 or P <0.01) ). In addition, the intracellular ROS was reduced by TSG (P <0.01) .Conclusions: TSG inhibited Ang II-induced VSMC proliferation. Its antiproliferative effect might be associated with down-regulation of intracellular ROS, followed by the suppression of the Src -MEK1 / 2-ERK1 / 2 signal pathway, and hence, blocking cell cycle progression.