Acute liver injury (ALI) refers to abnormalities in liver function caused by various causes and accompanied by poor prognosis and high mortality. Common predisposing factors for the disease are viral hepatitis, bacteria, alcohol, and certain hepatotoxic drugs. Inflammatory response and oxidative stress are critical for the pathogenesis of ALI. Pterostilbene (Pte), a natural polyphenol product extracted from blueberries and grapes, has been reported that exerted multiple biological activities, including antioxidative, anti-inflammatory, anti-carcinogenic, and anti-apoptotic properties. However, there is very little data showing the hepatoprotective effect of Pte on lipopolysaccharide/D-galactosamine (LPS/D-Gal)-induced ALI in mice. In this study, the possible protective effect and potential mechanisms of Pte on ALI are being investigated. It has been found that Pte markedly ameliorates LPS/D-Gal-induced inflammatory infiltration, hemorrhage, and dissociation of the hepatic cord, reducing the myeloperoxidase (MPO) activity in liver tissues and serum levels of alanine transaminase (ALT) and aspartate aminotransferase (AST) in ALI. Pte also inhibits LPS/D-Gal-induced secretion of pro-inflammatory cytokine tumor necrosis factor-a (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β) in liver tissues. Furthermore, the western blot analysis reveals that LPS/D-Gal-activated nuclear factor-kappa B (NF-κB) is significantly inhibited by Pte, and nuclear factor (erythroid-derived 2)–like 2 (Nrf2) and heme oxygenase-1 (HO-1) are upregulated by Pte. In conclusion, our results suggest that Pte exerts anti-inflammatory and antioxidative effects, which might contribute to ameliorating LPS/D-Gal-induced ALI in mice. Pte has the potential to be a preventive hepatoprotective agent.

急性肝损伤（ALI）是指各种原因引起的肝功能异常，预后差，死亡率高。该病的常见诱发因素是病毒性肝炎、细菌、酒精和某些肝毒性药物。炎症反应和氧化应激对于 ALI 的发病机制至关重要。紫檀 (Pte) 是一种从蓝莓和葡萄中提取的天然多酚产品，据报道具有多种生物活性，包括抗氧化、抗炎、抗癌和抗凋亡特性。然而，很少有数据显示 Pte 对脂多糖/D-半乳糖胺 (LPS/D-Gal) 诱导的小鼠 ALI 的保肝作用。在这项研究中，正在研究 Pte 对 ALI 可能的保护作用和潜在机制。已发现 Pte 显着改善 LPS/D-Gal 诱导的肝索炎症浸润、出血和解离，降低肝组织中髓过氧化物酶 (MPO) 活性和血清丙氨酸转氨酶 (ALT) 和天冬氨酸转氨酶水平。 AST）在阿里。Pte 还抑制 LPS/D-Gal 诱导的肝组织中促炎细胞因子肿瘤坏死因子-a (TNF-α)、白介素 6 (IL-6) 和白介素 1β (IL-1β) 的分泌。此外，蛋白质印迹分析显示 LPS/D-Gal 激活的核因子-κB (NF-κB) 被 Pte 显着抑制，核因子（红细胞衍生的 2）样 2（Nrf2）和血红素加氧酶- 1 (HO-1) 被 Pte 上调。总之，我们的结果表明 Pte 具有抗炎和抗氧化作用，这可能有助于改善小鼠 LPS/D-Gal 诱导的 ALI。Pte 有可能成为预防性肝保护剂。