ArticleMolecular medicine reports2020
Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Hepatic stellate cell inhibition by angiotensin II receptor blocker mitigates liver injury and fibrosis via NF-κB-galectin-3 suppression in a rat nonalcoholic steatohepatitis model.Archives of toxicology · 2025Article
- Effects and mechanisms of Zhizi Chuanxiong herb pair against atherosclerosis: an integration of network pharmacology, molecular docking, and experimental validation.Chinese medicine · 2024Article
- Mechanism of ferroptosis in breast cancer and research progress of natural compounds regulating ferroptosis.Journal of cellular and molecular medicine · 2024Review
- Exploring the role of Yuxuebi tablet in neuropathic pain with the method of similarity research of drug pharmacological effects based on unsupervised machine learning.Frontiers in pharmacology · 2024Article
- Levistolide a Attenuates Acute Kidney Injury in Mice by Inhibiting the TLR-4/NF-κB Pathway.Drug design, development and therapy · 2024Article
- Catalpol inhibits hepatic stellate cell activation by reducing the formation and changing the contents of hepatocyte-derived extracellular vesicles.Journal of cell communication and signaling · 2023Article
- Levistilide a Induces Ferroptosis by Activating the Nrf2/HO-1 Signaling Pathway in Breast Cancer Cells.Drug design, development and therapy · 2022Article
- Effects of Levistilide A on Hemorheology and Endothelial Cell Injury in Rats with Blood Stasis.Evidence-based complementary and alternative medicine : eCAM · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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