Drug Design, Development and Therapy (Feb 2020)

Inhibitory Effect of Curcumin on Artery Restenosis Following Carotid Endarterectomy and Its Associated Mechanism in vitro and in vivo

  • Zhang D,
  • Yang Y,
  • Li Y,
  • Zhang G,
  • Cheng Z

Journal volume & issue
Vol. Volume 14
pp. 855 – 866

Abstract

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Dapeng Zhang,1 Yanhui Yang,2 Yuanchao Li,1 Guodong Zhang,1 Zhenguo Cheng1 1Neurosurgery Department, Xinxiang Central Hospital, Xinxiang, Henan Province 453000, People’s Republic of China; 2Color Ultrasonic Room, People’s Hospital of Huixian, Xinxiang, Henan Province 453600, People’s Republic of ChinaCorrespondence: Zhenguo ChengNeurosurgery Department, Xinxiang Central Hospital, No. 56 Jinsui Street, Xinxiang, Henan Province 453000, People’s Republic of ChinaTel +86 156 3735 9907Email [email protected]: 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.Keywords: curcumin, carotid endarterectomy, restenosis, vascular smooth muscle cells, Raf/MEK/ERK

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