ArticleFEBS open bio2019
S-allyl-l-cysteine (SAC) protects hepatocytes from alcohol-induced apoptosis.
Article in FEBS open bio, 2019. 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, 20 citations in OpenAlex.
- Black Garlic: Evolution of the Chemical Composition and Broad Biological Activities.Journal of agricultural and food chemistry · 2025Review
- Tracing the Path from Obesity to Diabetes: How S-Allyl Cysteine Shapes Metabolic Health.Nutrients · 2025Review
- Aged Garlic Extract and Its Bioactive Molecules S-Allyl-Cysteine and S1-Propenyl-Cysteine: A Review Focusing on Evidences Supporting Their Use for Mitigating the Effects of Cigarette Smoking.Molecules (Basel, Switzerland) · 2025Review
- Methotrexate-induced hepatotoxicity in rats and the therapeutic properties of vitamin E: a histopathologic and flowcytometric research.Clinical and experimental hepatology · 2023Article
- Synthesis and Characterization of Plumbagin S-Allyl Cysteine Ester: Determination of Anticancer Activity In Silico and In Vitro.Applied biochemistry and biotechnology · 2022Article
- Preparation, Characterization, and In Vitro Evaluation of Inclusion Complexes Formed betweenACS omega · 2022Article
- Disrupted HAntioxidants (Basel, Switzerland) · 2021Review
- S-allyl-L-cysteine protects hepatocytes from indomethacin-induced apoptosis by attenuating endoplasmic reticulum stress.FEBS open bio · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte apoptosis is frequently observed in alcohol-related liver disease (ARLD), which ranks among the 30 leading causes of death worldwide. In the current study, we explored the impact of S-allyl-l-cysteine (SAC), an organosulfur component of garlic, on hepatocyte apoptosis induced by alcohol. Rat liver (BRL-3A) cells were challenged by ethanol with or without SAC treatment. Cell death/viability, reactive oxygen species (ROS) generation, mitochondrial Cytochrome C release, and caspase 3 activity were then examined. We found that ethanol remarkably induced apoptosis of hepatocytes, while SAC treatment rescued ethanol-induced hepatocyte injury, as demonstrated by cell counting kit-8 (CCK8) assay, TUNEL assay, and annexin V/PI staining assay. Ethanol evoked ROS generation in BRL-3A cells, and this was abated by SAC pretreatment, as indicated by 2',7'-dichlorofluorescin diacetate (DCFDA) staining assay. Moreover, ethanol suppressed cellular anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) expression, increased pro-apoptotic protein Bcl-2-associated X protein (Bax) expression, induced mitochondrial Cytochrome C release, and activated the caspase 3-dependent apoptosis pathway in BRL-3A cells. SAC was sufficient to abolish all these changes induced by ethanol, thereby revealing the molecular mechanisms underlying its protective effects. In conclusion, SAC protects hepatocytes from ethanol-induced apoptosis and may be suitable for use as a novel anti-apoptotic agent for treating ARLD.
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