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Protective Effects of Fisetin on Hepatic Ischemia-reperfusion Injury Through Alleviation of Apoptosis and Oxidative Stress.

非瑟酮通过减轻细胞凋亡和氧化应激对肝脏缺血再灌注损伤的保护作用。

  • 影响因子:2.10
  • DOI:10.1016/j.arcmed.2020.10.009
  • 作者列表:"Li Z","Wang Y","Zhang Y","Wang X","Gao B","Li Y","Li R","Wang J
  • 发表时间:2021-02-01
Abstract

BACKGROUND AND AIMS:Hepatic ischemia-reperfusion injury (IRI) is the main leading cause of morbidity and mortality of patients after liver surgery and transplantation. Fisetin, a kind of flavonoid, has been reported to protect against myocardial and cerebral IRI. However, the effects of fisetin on liver IRI were poorly investigated. METHODS:C57BL/6 mice were used to establish the liver IRI model in vivo. Intraperitoneal injection of fisetin was performed one hour before IR treatment (1 h ischemia and 6h reperfusion). In vitro experimental study was conducted using AML-12 hepatocytes with 1 h hypoxia and 12 h reoxygenation (HR) treatment. Tissue damage was evaluated through serum AST and ALT levels and hematoxylin-eosin (HE) staining. Cell apoptosis was assessed by TUNEL staining and protein levels of Bax, Bcl-2, cleaved-caspase-3, and cleaved-PARP. Oxidative stress was evaluated by ROS and MDA levels and the activity of SOD and GSH-Px. Immunohistochemistry and immunofluorescence assay were performed to observe the translocation of Nrf2 from the cytoplasm into the nucleus. RESULTS:The histopathological assessment showed that fisetin attenuated IR-induced liver damage obviously. Besides, fisetin served a protective role in IR liver to alleviate cell apoptosis and oxidative stress in vivo and in vitro. Introduction of high concentration of fisetin promoted the translocation of Nrf2 from the cytoplasm into the nucleus, increasing protein expression of its downstream elements, at least HO-1 in IR liver tissues and hepatocytes after HR. Inhibition of Nrf2 could reverse the effects of fisetin on cell viability, cell apoptosis, and also oxidative stress of HR hepatocytes, suggesting that Nrf2 signaling was necessary in fisetin-mediated regulations of liver IRI. CONCLUSION:Fisetin alleviates liver damage, cell apoptosis, and oxidative stress induced by liver IRI, at least through Nrf2/HO-1 signaling pathway, suggesting that fisetin could be considered as a targeted drug for liver IRI treatment.

摘要

背景和目的: 肝脏缺血再灌注损伤 (IRI) 是肝脏手术和移植后患者发病和死亡的主要原因。据报道,非瑟酮是一种黄酮类化合物,可预防心肌和脑IRI。然而,非瑟酮对肝脏IRI的影响研究很少。 方法: 采用C57BL/6小鼠建立体内肝脏IRI模型。在IR处理前1小时 (缺血1小时和再灌注6小时) 进行非瑟酮的腹膜内注射。用AML-12个肝细胞进行1 h缺氧和12 h复氧 (HR) 处理的体外实验研究。通过血清AST和ALT水平和苏木精-伊红 (HE) 染色评估组织损伤。通过TUNEL染色和Bax、Bcl-2、cleaved-caspase-3和cleaved-PARP的蛋白水平评估细胞凋亡。通过ROS和MDA水平以及SOD和GSH-Px活性评估氧化应激。采用免疫组织化学和免疫荧光方法观察Nrf2从细胞质向细胞核的转运情况。 结果: 组织病理学检查显示,非瑟酮明显减轻IR诱导的肝损伤。此外,非瑟酮在体内和体外对IR肝脏具有保护作用,以减轻细胞凋亡和氧化应激。引入高浓度的非瑟酮促进Nrf2从细胞质转位到细胞核中,增加其下游元件的蛋白表达,HR后IR肝组织和肝细胞中至少HO-1。抑制Nrf2可以逆转非瑟酮对细胞活力、细胞凋亡以及HR肝细胞氧化应激的影响,表明Nrf2信号在非瑟酮介导的肝脏IRI调节中是必要的。 结论: 非赛汀至少通过Nrf2/HO-1信号通路减轻肝脏IRI诱导的肝脏损伤、细胞凋亡和氧化应激,提示非赛汀可考虑作为肝脏IRI治疗的靶向药物。

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