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Inhibitory Effect of Curcumin on Artery Restenosis Following Carotid Endarterectomy and Its Associated Mechanism in vitro and in vivo
OBJECTIVE: The present study aimed to assess the effect of curcumin (Cur) on carotid artery restenosis following carotid endarterectomy (CEA) and its associated mechanism in vivo and in vitro. METHODS: Ang II was used to induce excessive proliferation of rabbit aortic smooth muscle cells (CCC-SMC-1)...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7049773/ https://www.ncbi.nlm.nih.gov/pubmed/32161445 http://dx.doi.org/10.2147/DDDT.S229607 |
Sumario: | OBJECTIVE: The present study aimed to assess the effect of curcumin (Cur) on carotid artery restenosis following carotid endarterectomy (CEA) and its associated mechanism in vivo and in vitro. METHODS: Ang II was used to induce excessive proliferation of rabbit aortic smooth muscle cells (CCC-SMC-1) in order to establish a hemadostenosis cell model. Similarly, the animal model of carotid artery restenosis was established by carotid artery gas drying injury combined with high-fat feed prior to CEA. CCC-SMC-1 cells and animals were treated by Cur and its effects on neointimal hyperplasia, inflammation and oxidative stress were detected and observed. The proteins that were associated with the Raf/MEK/ERK pathway were detected in cells and rabbit carotid artery tissues. RESULTS: Cur inhibited the proliferation of smooth muscle cells and neointimal formation and reduced the inflammation and oxidative stress indices. Concomitantly, Cur reduced the phosphorylation of the Raf/MEK/ERK pathway proteins. CONCLUSION: Cur could inhibit carotid restenosis following CEA by inhibiting the activation of the Raf/MEK/ERK pathway. |
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