ArticleAmerican journal of translational research2017
Therapeutic effect of rosuvastatin and propylthiouracil on ameliorating high-cholesterol diet-induced fatty liver disease, fibrosis and inflammation in rabbit.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Effect of Sun's Bushen Huayu formula on M1/M2-associated markers and endometrial repair in a thin endometrium model.Scientific reports · 2026Article
- A novel cardioprotective mechanism of rosuvastatin: restoring PINK1/parkin-mediated mitophagy via SIRT1/FOXO1 activation in doxorubicin-induced cardiotoxicity.Cancer chemotherapy and pharmacology · 2025Article
- Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data.Current pharmaceutical design · 2024Review
- Inhibition of Bruton's Tyrosine Kinase Protects Against Burn Sepsis-Induced Intestinal Injury.Frontiers in medicine · 2022Article
- Morin enhances hepatic Nrf2 expression in a liver fibrosis rat model.World journal of gastroenterology · 2017Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study tested the hypothesis that high-cholesterol diet (HCD)-induced fatty liver disease could be ameliorated by rosuvastatin (Ros) and propylthiouracil (PTU) therapy. Thirty-two Zealand rabbits were equally divided into group 1 (sham-control), group 2 (HCD for 8 weeks), group 3 [HCD-Ros (20 mg/kg/day administration after 4-week HFD for 4 weeks)], group 4 [HCD-PTU (0.1% PTU in drinking water) with treatment course as group 3]. Liver weight, fibrosis, collagen deposition area, and serum levels of AST/ALT were highest in group 2, lowest in group 1, and significantly higher in group 4 than group 3 (all P<0.0001). The levels of inflammatory (TNF-α/NF-κB/IL-1ß/IL-6/MMP-9/VCAM-1/PAI-1/TLR-4, MyD88/IL-12/IFN-γ), oxidative stress (NOX-1/NOX-2/oxidized protein), apoptotic (Bax/cleaved-capase-3/PARP), fibrotic (Smad-3/TGF-ß), and mitochondria-damaged (cytosolic-cytochrome-C) proteins showed an identical pattern, whereas antiapoptotic (Bcl-2), mitochondrial-integrity (mitochondrial-cytochrome-C) and antioxidative (SIRT1/SIRT3) biomarkers exhibited an opposite pattern to fibrosis among the four groups (all P<0.0001). The cellular expressions of inflammatory (Kupffer/CD14/CD44), α-fetoprotein-positively stained biomarkers, apoptotic nuclei and fat cells displayed an identical pattern to fibrosis (all P<0.0001). In conclusion, Ros-PTU therapy attenuated liver fibrosis, inflammatory reaction and generation of oxidative stress and fatty liver after HCD challenge in rabbits.
Indexed as
Identifiers
28861173PMC5575196W2984804986What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.