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首页> 外文期刊>Journal of biochemical and molecular toxicology >Does acetaminophen hepatotoxicity involve apoptosis, inflammatory liver injury, and lipid peroxidation?
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Does acetaminophen hepatotoxicity involve apoptosis, inflammatory liver injury, and lipid peroxidation?

机译：乙酰氨基酚肝毒性是否涉及细胞凋亡，炎症性肝损伤和脂质过氧化？

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Dear Editor, We read with interest a recent paper by Helal and Samra reporting the effect of irbesartan in a mouse model of acetaminophen (APAP)-induced liver injury. After a dose of 500 mg/kg APAP, the authors administered 50 or 75 mg/kg irbesartan at 1 and 12 h after APAP and measured a number of parameters related to injury and various mechanistic aspects at 24 h. The authors demonstrated profound protection (close to 100% based on plasma alanine ami-notransferase activities) and concluded that irbesartan treatment is safe due to its antiapoptotic, anti-inflammatory, and antioxidant activities. On the positive side, the authors used mice, which is a clinically relevant model, and administered the intervention after APAP, which is therapeutically relevant. However, we have concerns regarding the validity of the mechanistic conclusions because there is virtually no apoptotic cell death in this model; the inflammatory response does not contribute to the injury but is important for repair, and lipid peroxidation (LPO) is not a relevant cell injury mechanism in APAP hepatotoxicity. Our concern is not so much related to the use of irbesartan as an antidote against APAP-induced liver injury because there are other more promising drug candidates in development. We are concerned that this manuscript is just an example of the current trend of countless intervention studies that copy each other's experimental approach and conclusions, which in our opinion, are not justified by the data and, in most cases, are simply wrong.
机译：亲爱的编辑，我们饶有兴趣地阅读了Helal和Samra最近的一篇论文，报道了厄贝沙坦在对乙酰氨基酚（APAP）诱导的小鼠肝损伤模型中的作用。在剂量为500 mg/kg APAP后，作者在APAP后1小时和12小时服用50或75 mg/kg厄贝沙坦，并在24小时测量了许多与损伤相关的参数和各种机制方面。作者证明了深刻的保护作用（基于血浆丙氨酸氨基转移酶活性接近100%），并得出结论，厄贝沙坦治疗是安全的，因为其抗凋亡，抗炎和抗氧化活性。在积极的一面，作者使用了小鼠，这是一种临床相关的模型，并在APAP后进行干预，这与治疗相关。然而，我们对机制结论的有效性表示担忧，因为在这个模型中几乎没有凋亡细胞死亡；炎症反应不参与损伤，但对修复很重要，脂质过氧化（LPO）不是APAP肝毒性的相关细胞损伤机制。我们的担忧与厄贝沙坦作为APAP诱导的肝损伤解毒剂的使用无关，因为还有其他更具前景的候选药物正在研发中。我们担心的是，这份手稿只是当前无数干预研究趋势的一个例子，它们相互复制对方的实验方法和结论，在我们看来，这些方法和结论没有数据依据，而且在大多数情况下都是错误的。

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