Author/Authors :
Lu, Ming Department of Cardiology - the Second Affiliated Hospital of Zhejiang Chinese Medical University - Hangzhou - Zhejiang, China , Luo, Ying Department of Cardiology - the Second Affiliated Hospital of Zhejiang Chinese Medical University - Hangzhou - Zhejiang, China , Hu, Pengfei Department of Cardiology - the Second Affiliated Hospital of Zhejiang Chinese Medical University - Hangzhou - Zhejiang, China , Dou, Liping Department of Cardiology - the Second Affiliated Hospital of Zhejiang Chinese Medical University - Hangzhou - Zhejiang, China , Huang, Shuwei Department of Cardiology - the Second Affiliated Hospital of Zhejiang Chinese Medical University - Hangzhou - Zhejiang, China
Abstract :
Objective(s): Vascular smooth muscle cells (VSMCs) play a key role in the pathogenesis of diabetic vascular disease. Our current study sought to explore the effects of tanshinone IIA on the proliferation and migration of VSMCs induced by advanced glycation end products (AGEs). Materials and Methods: In this study, we examined the effects of tanshinone IIA by cell proliferation assay and cell migration assay. and we explored the underlying mechanism by Western blotting.
Results: AGEs significantly induced the proliferation and migration of VSMCs, but treatment with tanshinone IIA attenuated these effects. AGEs could increase the activity of the ERK1/2 and p38 pathways but not the JNK pathway. Treatment with tanshinone IIA inhibited the AGEs-induced activation of the ERK1/2 pathway but not the p38 pathway. Conclusion: Tanshinone IIA inhibits AGEs-induced proliferation and migration of VSMCs by suppressing the ERK1/2 MAPK signaling pathway.
Keywords :
Advanced , ERK1/2 , JNK , P38 , Tanshinone IIA , Vascular Smooth Muscle