ArticleDrug design, development and therapy2019
Emodin-induced autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes.
Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- Shufeng Jiedu, a promising herbal therapy for moderate COVID-19:Antiviral and anti-inflammatory properties, pathways of bioactive compounds, and a clinical real-world pragmatic study.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2021Trial
- Hepatotoxic Compounds and Mechanisms of Polygonum Multiflorum: A Narrative Review of Recent Advances.International journal of molecular sciences · 2026Review
- Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.Current medical science · 2026Review
- Plant secondary metabolites exert therapeutic effects by modulating autophagy pathways.Frontiers in plant science · 2026Review
- Mechanistic insights into the multi-target anti-atherosclerotic actions of rhubarb: a traditional remedy revisited.Chinese medicine · 2025Review
- Protective efficacy of emodin in Swiss Albino mice induced with Dalton Ascitic lymphoma.3 Biotech · 2025Article
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- Tailoring traditional Chinese medicine in cancer therapy.Molecular cancer · 2025Review
- FEZF1-AS1 drives autophagy-mediated progression of colon cancer and reduces chemosensitivity through inhabiting the PI3K/AKT/mTOR signaling pathway.Frontiers in genetics · 2025Article
- Review
- Chrysin-loaded PEGylated liposomes protect against alloxan-induced diabetic neuropathy in rats: the interplay between endoplasmic reticulum stress and autophagy.Biological research · 2024Article
- Emodin alleviates intestinal ischemia-reperfusion injury through antioxidant stress, anti-inflammatory responses and anti-apoptosis effects via Akt-mediated HO-1 upregulation.Journal of inflammation (London, England) · 2024Article
- The Anthraquinone Derivative C2 Enhances Oxaliplatin-Induced Cell Death and Triggers Autophagy via the PI3K/AKT/mTOR Pathway.International journal of molecular sciences · 2024Article
- Inhibiting Liver Autophagy and Promoting Hepatocyte Apoptosis byTropical medicine and infectious disease · 2024Article
- Emodin Ameliorates High Glucose-Induced Podocyte Apoptosis via Regulating AMPK/mTOR-Mediated Autophagy Signaling Pathway.Chinese journal of integrative medicine · 2023Article
- Trained immunity in monocyte/macrophage: Novel mechanism of phytochemicals in the treatment of atherosclerotic cardiovascular disease.Frontiers in pharmacology · 2023Review
- Hepatoprotective agents in the management of intrahepatic cholestasis of pregnancy: current knowledge and prospects.Frontiers in pharmacology · 2023Review
- Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases.Frontiers in pharmacology · 2023Review
- A Network-Pharmacology-Combined Integrated Pharmacokinetic Strategy to Investigate the Mechanism of Potential Liver Injury due toMolecules (Basel, Switzerland) · 2022Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEmodin, a major component of
methodsThe present study used the normal human liver cell line L02 to investigate the effects and mechanisms of emodin in hepatic cells. After treatment with emodin, L02 cells were examined for viability, apoptosis and autophagy with the Cell Counting Kit-8 (CCK-8), annexin V/PerCP staining and GFP-LC3 plasmid transfection. The expression of proteins including cleaved caspase-3, LC3B-I/II, p-PI3K, PI3K, p-AKT, AKT, p-mTOR, mTOR and actin was examined by using Western blot.
resultsEmodin significantly inhibited the viability of and induced apoptosis in L02 cells in a dose- and time-dependent manner. In addition, emodin increased the number of GFP-LC3 puncta in L02 cells and upregulated the expression of LC3B-II compared to those in control cells. Furthermore, emodin significantly decreased the expression of p-PI3K, p-AKT and p-mTOR in a dose-dependent manner compared to that in control cells without altering the expression of PI3K, AKT and mTOR. Notably, cotreatment with emodin and 3-methyladenine (3-MA) or rapamycin significantly increased and decreased the apoptosis rate of L02 cells, respectively, compared to that of cells treated with emodin alone.
conclusionIn conclusion, emodin exhibited cytotoxicity in the L02 human hepatic cell line by promoting apoptosis, and it also induced autophagy through the suppression of the PI3K/AKT/mTOR signalling pathway. The autophagy could play a protective role following emodin treatment.
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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.