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首页> 外文期刊>Journal of Cellular Physiology >Neutrophil extracellular traps in acrolein promoted hepatic ischemia reperfusion injury: Therapeutic potential of NOX2 and p38MAPK inhibitors
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Neutrophil extracellular traps in acrolein promoted hepatic ischemia reperfusion injury: Therapeutic potential of NOX2 and p38MAPK inhibitors

机译：中性粒细胞胞外陷阱在丙烯醛促进肝缺血再灌注损伤:NOX2和p38MAPK的治疗潜力抑制剂

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Neutrophil is a significant contributor to ischemia reperfusion (IR) induced liver tissue damage. However, the exact role of neutrophils in IR induced innate immune activation and liver damage is not quite clear. Our study sheds light on the role of chronic oxidative stress end products in worsening the IR inflammatory process by neutrophil recruitment and activation following liver surgery. We employed specific inhibitors for molecular targets—NOX2 (NADPH oxidase 2) and P38 MAPK (Mitogen activated protein kinase) signal to counteract neutrophil activation and neutrophil extracellular trap (NET) release induced liver damage in IR injury. We found that acrolein initiated neutrophil chemotaxis and induced NET release both in vitro and in vivo. Acrolein exposure caused NET induced nuclear and mitochondrial damage in HepG2 cells as well as aggravated the IR injury in rat liver. Pretreatment with F‐apocynin and naringin, efficiently suppressed acrolein induced NET release in vitro. Notably, it suppressed the expression of inflammatory cytokines, P38MAPK‐ERK activation, and apoptotic signals in rat liver exposed to acrolein and subjected to IR. Moreover, this combination effectively attenuated acrolein induced NET release and hepatic IR injury. In the current study we have shown that the acrolein accumulation in liver due to chronic stress, is responsible for neutrophil recruitment and its activation leading to NET induced liver damage during surgery. Our study shows that therapeutic targeting of NOX2 and P38MAPK signaling in patients with chronic hepatic disorders would improve post operative hepatic function and survival.
机译：中性粒细胞是一个重大的因素缺血再灌注(IR)诱导肝组织损害。红外感应先天免疫激活和肝脏损害是不清楚的。在慢性氧化应激的作用产品红外炎症恶化过程中性粒细胞招募和激活肝脏手术后。抑制剂分子targets-NOX2 (NADPH氧化酶2)和P38 MAPK(有丝分裂原激活蛋白激酶)信号抵消嗜中性粒细胞激活和嗜中性粒细胞胞外陷阱(净)释放红外损伤诱导肝损伤。我们发现,丙烯醛发起嗜中性粒细胞趋化作用和诱导净释放出体外和体内。HepG2细胞的核和线粒体损伤以及加重红外损伤大鼠肝脏。预处理和F apocynin和柚皮苷,有效地抑制丙烯醛诱导净体外释放。的炎性细胞因子的表达,P38MAPK兵激活,并在大鼠肝脏凋亡信号暴露在丙烯醛和IR。此外,这种组合有效地衰减丙烯醛净释放和肝红外感应受伤。由于慢性丙烯醛积累在肝脏压力,负责招募中性粒细胞和它的激活导致净诱导肝脏在手术过程中损坏。治疗目标NOX2 P38MAPK信号在慢性肝患者疾病将会改善术后肝功能和生存。

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