ArticleMedical science monitor : international medical journal of experimental and clinical research2012
18α-Glycyrrhizin induces apoptosis and suppresses activation of rat hepatic stellate cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Efficacy and safety of glycyrrhizic acid preparation treating comorbid liver injury in COVID-19: A systematic review.Frontiers in pharmacology · 2022Pooled it
- Mechanisms and therapeutic potential of glycyrrhizic acid: Insights into key signaling pathways and disease modulation (Review).Molecular medicine reports · 2026Review
- Glycyrrhizin preparations in liver diseases: a narrative review of mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Magnesium isoglycyrrhizinate prevented the liver injury of acetaminophen by promoting mitochondrial biogenesis.Toxicology research · 2025Article
- Synthesis, Antiviral, and Antibacterial Activity of the Glycyrrhizic Acid and Glycyrrhetinic Acid Derivatives.Russian journal of bioorganic chemistry · 2022Article
- The Role of Cancer-Associated Fibroblasts in Hepatocellular Carcinoma and the Value of Traditional Chinese Medicine Treatment.Frontiers in oncology · 2021Review
- MicroRNA-34a Promotes Hepatic Stellate Cell Activation via Targeting ACSL1.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Synthesis and discovery of 18α-GAMG as anticancer agent in vitro and in vivo via down expression of protein p65.Scientific reports · 2014Article
- Synthesis, molecular docking and biological evaluation of glycyrrhizin analogs as anticancer agents targeting EGFR.Molecules (Basel, Switzerland) · 2014Article
- Protective mechanisms of medicinal plants targeting hepatic stellate cell activation and extracellular matrix deposition in liver fibrosis.Chinese medicine · 2014Article
- Liver fibrosis and protection mechanisms action of medicinal plants targeting apoptosis of hepatocytes and hepatic stellate cells.Advances in pharmacological sciences · 2014Review
- Herbal products: benefits, limits, and applications in chronic liver disease.Evidence-based complementary and alternative medicine : eCAM · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigate the potential mechanisms underlying the protective effects of 18α Glycyrrhizin (GL) on rat hepatic stellate cells (HSCs) and hepatocytes in vivo and in vitro. MATERIAL/
methodsSprague-Dawley (SD) rats were randomly divided into 5 groups: normal control group, liver fibrosis group, high-dose 18α GL group (25 mg/ kg/d), intermediate-dose 18α GL group (12.5 mg/kg/d) and low-dose 18α GL group (6.25 mg/ kg/d). The rat liver fibrosis model was induced by carbon tetrachloride (CCl4). The expressions of alpha-smooth muscle actin (αSMA) and NF-kappaB were determined by real-time PCR and immunohistochemistry.
results18αGL dose-dependently inhibited the CCl4-induced liver fibrosis. There were significant differences in the mRNA and protein expressions of αSMA between the fibrosis group and 18α-GL treatment groups, suggesting that 18α GL can suppress the proliferation and activation of HSCs. Few HSCs were apoptotic in the portal area and fibrous septum in the liver fibrosis group. However, the double-color staining of a-SMA and TUNEL showed that 18α-GL treatment groups increased HSC apoptosis. NF-kappaB was mainly found in the nucleus in the fibrosis group, while cytoplasmic expression of NF-kappaB was noted in the 18αGL groups. In the in vitro experiments, 18α GL promoted the proliferation of hepatocytes, but inhibited that of HSCs. HSCs were arrested in the G2/M phase following 18α GL treatment and were largely apoptotic.
conclusions18α-GL can suppress the activation of HSCs and induce the apoptosis of HSCs by blocking the translocation of NF-kappaB into the nucleus, which plays an important role in the protective effect of 18α-GL on liver fibrosis.
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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.