Liver damage induced by ischemia/reperfusion (I/R) remains a primary issue in liver transplantation and resection. Alpinetin, a novel plant flavonoid derived from Alpinia katsumadai Hayata, is widely used to treat various inflammatory diseases. However, the effects of alpinetin on hepatic I/R injury remain unclear. The present study investigated the protective effects of alpinetin pretreatment on hepatic I/R injury in mice. C57BL/6 mice were subjected to 1 h of partial hepatic ischemia followed by 6 h of reperfusion. Alpinetin (50 mg/kg) was given by intraperitoneal injection 1 h before liver ischemia. The blood and liver tissues were collected to assess biochemical indicators, hepatocyte damage, and levels of proteins related to signaling pathways. Furthermore, a hepatocytes hypoxia/reoxygenation (H/R) model was established for in vitro experiments. In vivo, we observed that alpinetin significantly attenuated the increases in alanine aminotransferase, aspartate transaminase, proinflammatory cytokines, hepatocyte damage, and apoptosis caused by hepatic I/R. Moreover, the hepatic I/R-induced nuclear factor kappa-B (NF-κB)/mitogen-activated protein kinase (MAPK) pathways were suppressed by alpinetin. In vitro, we also observed that alpinetin inhibited the inflammatory response, apoptosis, and activation of the NF-κB/MAPK pathways in hepatocytes after H/R treatment. Our data indicate that alpinetin ameliorated the inflammatory response and apoptosis induced by hepatic I/R injury in mice. The protective effects of alpinetin on hepatic I/R injury may be due to its ability to inhibit the NF-κB/MAPK signaling pathways. These results suggest that alpinetin is a promising potential therapeutic reagent for hepatic I/R injury.

缺血/再灌注（I / R）引起的肝损伤仍然是肝移植和切除术中的主要问题。Alpinetin，一种源自胜羽草的新型植物类黄酮Hayata被广泛用于治疗各种炎症性疾病。然而，尚不清楚阿尔卑斯素对肝I / R损伤的作用。本研究调查了高山素预处理对小鼠肝I / R损伤的保护作用。使C57BL / 6小鼠经历1 h的部分肝缺血，然后再灌注6 h。肝缺血前1 h腹腔注射Alpinetin（50 mg / kg）。收集血液和肝脏组织以评估生化指标，肝细胞损伤以及与信号通路相关的蛋白质水平。此外，建立了肝细胞缺氧/复氧（H / R）模型用于体外实验。体内，我们观察到阿尔卑斯素显着减轻了丙氨酸转氨酶，天冬氨酸转氨酶，促炎细胞因子，肝细胞损伤和肝I / R引起的细胞凋亡的增加。此外，alpinetin抑制了肝I / R诱导的核因子kappa-B（NF-κB）/丝裂原激活的蛋白激酶（MAPK）通路。体外，我们还观察到Alpinetin抑制了H / R治疗后肝细胞的炎症反应，细胞凋亡和NF-κB/ MAPK通路的激活。我们的数据表明，alpinetin改善了小鼠肝脏I / R损伤引起的炎症反应和细胞凋亡。Alpinetin对肝I / R损伤的保护作用可能是由于其抑制NF-κB/ MAPK信号通路的能力。这些结果表明，alpinetin是治疗肝I / R损伤的有前途的潜在治疗剂。