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S-allyl-l-cysteine (SAC) Protects Hepatocytes From Alcohol-Induced Apoptosis

S-allyl-l-cysteine (SAC) Protects Hepatocytes From Alcohol-Induced Apoptosis

Peng Chen, Mingdao Hu, Feng Liu, Henghai Yu, Chen Chen

FEBS Open Bio. 2019 Jul;9(7):1327-1336.

PMID: 31161729

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP21593771	S-Allyl-L-cysteine		21593-77-1	Price

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