Journal
IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES
Volume 21, Issue 1, Pages 83-88Publisher
MASHHAD UNIV MED SCIENCES
DOI: 10.22038/IJBMS.2017.20100.5276
Keywords
Advanced; ERK1/2; Glycation end products; JNK; P38; Tanshinone IIA; Vascular Smooth Muscle
Funding
- Science Foundation of Health Bureau of Zhejiang Province [2015KYB273]
- Natural Science Foundation of Zhejiang Province [Y13H020030]
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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.
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