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首页> 外文期刊>FEBS Open Bio >S‐allyl‐l‐cysteine (SAC) protects hepatocytes from alcohol‐induced apoptosis
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S‐allyl‐l‐cysteine (SAC) protects hepatocytes from alcohol‐induced apoptosis

机译：S-烯丙基-L-半胱氨酸（SAC）保护肝细胞免受酒精诱导的凋亡

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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.
机译：在酒精相关性肝病（ARLD）中经常观察到肝细胞凋亡，它是全球30种主要死亡原因之一。在当前的研究中，我们探讨了大蒜中有机硫成分S-烯丙基-半胱氨酸（SAC）对酒精诱导的肝细胞凋亡的影响。在有或没有SAC处理的情况下，乙醇都会刺激大鼠肝（BRL-3A）细胞。然后检查细胞死亡/生存力，活性氧（ROS）生成，线粒体细胞色素C释放和caspase 3活性。我们发现乙醇显着诱导了肝细胞凋亡，而SAC处理挽救了乙醇诱导的肝细胞损伤，如细胞计数试剂盒8（CCK8）测定，TUNEL测定和膜联蛋白V / PI染色测定所证明。乙醇在BRL-3A细胞中引起ROS生成，并且通过2'，7'-二氯荧光素双乙酸盐（DCFDA）染色试验表明，通过SAC预处理可以减轻这种情况。此外，乙醇抑制细胞抗凋亡蛋白B细胞淋巴瘤2（Bcl-2）的表达，增加促凋亡蛋白Bcl-2相关X蛋白（Bax）的表达，诱导线粒体细胞色素C释放，并激活胱天蛋白酶3 BRL-3A细胞中的依赖凋亡途径。 SAC足以消除乙醇诱导的所有这些变化，从而揭示了其保护作用的分子机制。总之，SAC保护肝细胞免受乙醇诱导的凋亡，可能适合用作治疗ARLD的新型抗凋亡药物。

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