Sepsis is a severe disease, with high mortality. Permanent organ damage caused by sepsis reduces the quality of life of surviving patients. The liver is an easily damaged organ in sepsis and sepsis‑associated liver injury foretells a poor prognosis. Unfortunately, there are no effective treatments or drugs to solve this problem. Therefore, strategies or novel drugs are urgently required to protect against liver dysfunction in sepsis. In the present study, lipopolysaccharide (LPS) was used to establish a model of liver injury in vitro. The data demonstrated that pretreatment of L02 human normal hepatocytes with paeonol (PAE) alleviated LPS‑induced cell injury and decreased the levels of alanine aminotransferase and aspartate transaminase, indicating a protective effect of PAE. Further experiments demonstrated that PAE increased LPS‑decreased L02 cell viability, the levels of superoxide dismutase and Bcl‑2 expression. PAE decreased LPS‑increased cell apoptosis, intracellular reactive oxygen species and the expression levels of Bax and cleaved‑caspase‑3. PAE decreased LPS‑promoted mitochondrial depolarization and nuclear translocation of NF‑κB. In conclusion, PAE alleviated LPS‑induced liver injury via alteration of mitochondrial function and NF‑κB translocation. Therefore, PAE has potential for the treatment of sepsis.

中文翻译：

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Paeonol 通过改变线粒体功能和 NF-κB 易位来减轻脂多糖诱导的肝细胞损伤。

脓毒症是一种严重的疾病，死亡率很高。脓毒症引起的永久性器官损伤会降低幸存患者的生活质量。肝脏是脓毒症中容易受损的器官，脓毒症相关肝损伤预示预后不良。不幸的是，没有有效的治疗方法或药物来解决这个问题。因此，迫切需要策略或新药来预防脓毒症中的肝功能障碍。本研究采用脂多糖（LPS）建立体外肝损伤模型。. 数据表明，用丹皮酚 (PAE) 预处理 L02 人正常肝细胞可减轻 LPS 诱导的细胞损伤，并降低丙氨酸氨基转移酶和天冬氨酸转氨酶的水平，表明 PAE 具有保护作用。进一步的实验表明，PAE 增加了 LPS 降低的 L02 细胞活力、超氧化物歧化酶水平和 Bcl-2 表达。PAE 降低 LPS 增加的细胞凋亡、细胞内活性氧以及 Bax 和 cleaved-caspase-3 的表达水平。PAE 降低了 LPS 促进的线粒体去极化和 NF-κB 的核转位。总之，PAE 通过改变线粒体功能和 NF-κB 易位来减轻 LPS 诱导的肝损伤。因此，PAE具有治疗脓毒症的潜力。