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Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation

  • Authors:
    • Shu Li
    • Wei Zhao
    • Zhimin Zhao
    • Binbin Cheng
    • Shuang Li
    • Chenghai Liu
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology, Baoshan Branch, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201900, P.R. China, Institute of Liver Diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China, Department of Tradition Chinese Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2191-2198
    |
    Published online on: July 10, 2020
       https://doi.org/10.3892/mmr.2020.11326
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Abstract

The renin angiotensin system (RAS) serves an important role in the development of hepatic fibrosis. Therefore, the present study investigated the effect of levistilide A (Lev A) on hepatic fibrosis via regulation of RAS. The effects of Lev A on the proliferation and activation of hepatic stellate cells (HSCs) were measured using a 5‑ethynyl‑2'‑deoxyuridine assay, western blot analysis and immunofluorescence. The in vivo anti‑hepatic fibrosis effect of Lev A was examined using a CCL4‑induced rat fibrosis model. Lev A significantly prohibited angiotensin (Ang) II‑induced proliferation of HSCs, and overexpression of smooth muscle α‑actin (α‑SMA) and F‑actin in HSCs. Lev A partly reversed Ang II‑induced angiotensin type 1 receptor (AT1R) upregulation and ERK and c‑Jun phosphorylation. In CCL4‑induced hepatic fibrosis rats, Lev A treatment significantly decreased the expression of collagen, α‑SMA and hydroxyproline in rat liver, and improved liver functions. Lev A treatment also significantly inhibited the CCL4‑induced increase in plasma Ang II, and upregulation of AT1R and phosphorylated ERK in rat liver. In conclusion, Lev A is a potential agent for the treatment of hepatic fibrosis by suppressing Ang II/AT1R/ERK/c‑Jun activation in HSCs.
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Copy and paste a formatted citation
Spandidos Publications style
Li S, Zhao W, Zhao Z, Cheng B, Li S and Liu C: Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation. Mol Med Rep 22: 2191-2198, 2020.
APA
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., & Liu, C. (2020). Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation. Molecular Medicine Reports, 22, 2191-2198. https://doi.org/10.3892/mmr.2020.11326
MLA
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., Liu, C."Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation". Molecular Medicine Reports 22.3 (2020): 2191-2198.
Chicago
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., Liu, C."Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation". Molecular Medicine Reports 22, no. 3 (2020): 2191-2198. https://doi.org/10.3892/mmr.2020.11326
Copy and paste a formatted citation
x
Spandidos Publications style
Li S, Zhao W, Zhao Z, Cheng B, Li S and Liu C: Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation. Mol Med Rep 22: 2191-2198, 2020.
APA
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., & Liu, C. (2020). Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation. Molecular Medicine Reports, 22, 2191-2198. https://doi.org/10.3892/mmr.2020.11326
MLA
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., Liu, C."Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation". Molecular Medicine Reports 22.3 (2020): 2191-2198.
Chicago
Li, S., Zhao, W., Zhao, Z., Cheng, B., Li, S., Liu, C."Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation". Molecular Medicine Reports 22, no. 3 (2020): 2191-2198. https://doi.org/10.3892/mmr.2020.11326
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