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Article

Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy

  • Authors:
    • Xian‑Jie Xu
    • Wei‑Bo Zhao
    • Shi‑Bin Feng
    • Cheng Sun
    • Qiang Chen
    • Bing Ni
    • Hou‑Yuan Hu
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China, Department of Pathophysiology and High Altitude Pathology, Third Military Medical University, Chongqing 400038, P.R. China
  • Pages: 7657-7664
    |
    Published online on: September 20, 2017
       https://doi.org/10.3892/mmr.2017.7533
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Abstract

Reactive oxygen species (ROS) production has been implicated in the promotion of cellular senescence. Celastrol, a quinone methide triterpenoid isolated from the Celastraceae family, exerts antioxidant effects and enhances autophagy in various cell types. Since autophagy serves an important role in regulating ROS, it was hypothesized that the antioxidant effect of celastrol is via enhanced autophagy, thus inhibiting cell senescence. Therefore, the present study used a Senescence β‑Galactosidase Staining kit, western blot analysis and cell cycle analysis to investigate whether celastrol alleviates angiotensin (Ang) II‑induced cellular senescence by upregulating autophagy in vascular smooth muscle cells (VSMCs). The results demonstrated that celastrol reduced Ang II‑induced senescence of VSMCs. Ang II‑induced generation of ROS and the subsequent VSMC senescence were counteracted by pretreatment with celastrol, determined by a ROS assay kit. Celastrol significantly upregulated VSMC autophagy, which reduced intracellular ROS and the subsequent cellular senescence induced by Ang II. Furthermore, celastrol markedly suppressed activity of the mechanistic target of rapamycin signaling pathway in VSMCs. In conclusion, the present study demonstrated that celastrol counteracts VSMC senescence probably by reducing ROS production via activation of autophagy, which may hold promise for the prevention and treatment of aging‑associated cardiovascular disorders such as atherosclerosis.
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Copy and paste a formatted citation
Spandidos Publications style
Xu XJ, Zhao WB, Feng SB, Sun C, Chen Q, Ni B and Hu HY: Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy. Mol Med Rep 16: 7657-7664, 2017.
APA
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., & Hu, H. (2017). Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy. Molecular Medicine Reports, 16, 7657-7664. https://doi.org/10.3892/mmr.2017.7533
MLA
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., Hu, H."Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy". Molecular Medicine Reports 16.5 (2017): 7657-7664.
Chicago
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., Hu, H."Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy". Molecular Medicine Reports 16, no. 5 (2017): 7657-7664. https://doi.org/10.3892/mmr.2017.7533
Copy and paste a formatted citation
x
Spandidos Publications style
Xu XJ, Zhao WB, Feng SB, Sun C, Chen Q, Ni B and Hu HY: Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy. Mol Med Rep 16: 7657-7664, 2017.
APA
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., & Hu, H. (2017). Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy. Molecular Medicine Reports, 16, 7657-7664. https://doi.org/10.3892/mmr.2017.7533
MLA
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., Hu, H."Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy". Molecular Medicine Reports 16.5 (2017): 7657-7664.
Chicago
Xu, X., Zhao, W., Feng, S., Sun, C., Chen, Q., Ni, B., Hu, H."Celastrol alleviates angiotensin II‑mediated vascular smooth muscle cell senescence via induction of autophagy". Molecular Medicine Reports 16, no. 5 (2017): 7657-7664. https://doi.org/10.3892/mmr.2017.7533
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