1.Hydroxysafflor yellow A inhibits VSMCs proliferation via PCNA and MEK-ERK1/2
Jingshan ZHAO ; Mingxing FANG ; Qianyu GUO ; Yunfeng LI ; Bingyuan XU ; Shaohong LAI ; Shangyue ZHANG ; Yu LIU ; Aiying LI
Chinese Pharmacological Bulletin 2015;(7):984-987,988
Abstrac:Aim To study the effect of hydroxysafflor yellow A ( HYSA ) on the proliferation of vascular smooth muscle cells ( VSMCs) and the related molecu-lar mechanism. Methods The inhibitory effects of hydroxysafflor yellow A on VSMC proliferation was de-tected using cell culture, MTT assay, Western blot and immunohistochemical staining. Results The results showed that HYSA inhibited cell proliferation induced by PDGF in a dose-dependent (5,10,20,40 μmol· L-1 ) manner, reduced proliferating cell nuclear anti-gen ( PCNA ) expression and blocked PDGFR-MEK-ERK1/2 signaling pathway activated by PDGF in VSMCs. Conclusion HYSA inhibits VSMCs prolifer-ation via reducing the expression of PCNA and blocking signal transduction of MEK-ERK1/2 in VSMCs.
2.Hydroxysafflor yellow A inhibits rat vascular smooth muscle cells proliferation possibly via blocking signal transduction of MEK-ERK1/2
Jingshan ZHAO ; Qianyu GUO ; Shaohong LAI ; Shangyue ZHANG ; Hongli HAN
Chinese Journal of Cardiology 2015;43(8):728-731
Objective To elucidate the effect of hydroxysafflor yellow A (HYSA) on the proliferation of vascular smooth muscle cells (VSMCs) and the related mechanism.Methods VSMCs derived from SD rats were treated with DMEC culture medium (Control),10 ng/ml PDGF (PDGF group),pretreatment with HYSA at different doses (1,5,10,20,40,60 μmol/L) for 24 h then cotreatment with PDGF.After 24 h,MTT assay,Western blot and immunohistochemical staining were performed to evaluate the inhibitory effects of HYSA on VSMCs proliferation.Results HYSA inhibited PDGF induced VSMCs proliferation in a dose-dependent manner,dowregulated proliferating cell nuclear antigen (PCNA) expression and blocked PDGF activated PDGFR-MEK-ERK1/2 signaling pathway.Conclusions HYSA inhibits VSMCs proliferation possibly via downregulating the expression of PCNA and blocking MEK-ERK1/2 signal transduction in VSMCs.