PDF(Pubmed)
Abstract：
UNASSIGNED: The purpose of the present study was to investigate the effect of erythropoietin (EPO) on lung ischemia-reperfusion injury (LIRI).
UNASSIGNED: Sprague Dawley rats and BEAS-2B cells were employed to construct an ischemia-reperfusion (I/R)-induced model in vivo and in vitro, respectively. Afterward, I/R rats and tert-butyl hydroperoxide (TBHP)-induced cells were treated with different concentrations of EPO. Furthermore, 40 patients with LIRI and healthy controls were enrolled in the study.
UNASSIGNED: It was observed that lung tissue damage, cell apoptosis and the expression of BAX and caspase-3 were higher in the LIRI model in vivo and in vitro than in the control group, nevertheless, the Bcl-2, FGF23 and FGFR4 expression level was lower than in the control group. EPO administration significantly reduced lung tissue damage and cell apoptosis while also up-regulating the expression of FGF23 and FGFR4. Rescue experiments indicated that EPO exerted a protective role associated with the FGF23/FGFR4/p-ERK1/2 signal pathway. Notably, the expression of serum EPO, FGF23, FGFR4 and Bcl-2 was decreased in patients with LIRI, while the expression of caspase-3 and BAX was higher.
UNASSIGNED: EPO could effectively improve LIRI, which might be related to the activation of the FGF23/FGFR4/p-ERK1/2 signaling pathway.
UNASSIGNED: Sprague Dawley rats and BEAS-2B cells were employed to construct an ischemia-reperfusion (I/R)-induced model in vivo and in vitro, respectively. Afterward, I/R rats and tert-butyl hydroperoxide (TBHP)-induced cells were treated with different concentrations of EPO. Furthermore, 40 patients with LIRI and healthy controls were enrolled in the study.
UNASSIGNED: It was observed that lung tissue damage, cell apoptosis and the expression of BAX and caspase-3 were higher in the LIRI model in vivo and in vitro than in the control group, nevertheless, the Bcl-2, FGF23 and FGFR4 expression level was lower than in the control group. EPO administration significantly reduced lung tissue damage and cell apoptosis while also up-regulating the expression of FGF23 and FGFR4. Rescue experiments indicated that EPO exerted a protective role associated with the FGF23/FGFR4/p-ERK1/2 signal pathway. Notably, the expression of serum EPO, FGF23, FGFR4 and Bcl-2 was decreased in patients with LIRI, while the expression of caspase-3 and BAX was higher.
UNASSIGNED: EPO could effectively improve LIRI, which might be related to the activation of the FGF23/FGFR4/p-ERK1/2 signaling pathway.
摘要：
■本研究的目的是研究促红细胞生成素（EPO）对肺缺血再灌注损伤（LIRI）的影响。
■采用SpragueDawley大鼠和BEAS-2B细胞构建体内和体外缺血再灌注（I/R）诱导的模型，分别。之后,用不同浓度的EPO处理I/R大鼠和叔丁基过氧化氢(TBHP)诱导的细胞。此外，40名LIRI患者和健康对照者被纳入研究。
■观察到肺组织损伤，LIRI模型在体内和体外的细胞凋亡和BAX和caspase-3的表达均高于对照组，然而，Bcl-2、FGF23和FGFR4表达水平低于对照组。EPO给药可显着减少肺组织损伤和细胞凋亡，同时也上调FGF23和FGFR4的表达。挽救实验表明，EPO发挥了与FGF23/FGFR4/p-ERK1/2信号通路相关的保护作用。值得注意的是,血清EPO的表达,LIRI患者FGF23、FGFR4和Bcl-2降低,而caspase-3和BAX的表达较高。
■EPO可以有效提高LIRI，这可能与FGF23/FGFR4/p-ERK1/2信号通路的激活有关。
■采用SpragueDawley大鼠和BEAS-2B细胞构建体内和体外缺血再灌注（I/R）诱导的模型，分别。之后,用不同浓度的EPO处理I/R大鼠和叔丁基过氧化氢(TBHP)诱导的细胞。此外，40名LIRI患者和健康对照者被纳入研究。
■观察到肺组织损伤，LIRI模型在体内和体外的细胞凋亡和BAX和caspase-3的表达均高于对照组，然而，Bcl-2、FGF23和FGFR4表达水平低于对照组。EPO给药可显着减少肺组织损伤和细胞凋亡，同时也上调FGF23和FGFR4的表达。挽救实验表明，EPO发挥了与FGF23/FGFR4/p-ERK1/2信号通路相关的保护作用。值得注意的是,血清EPO的表达,LIRI患者FGF23、FGFR4和Bcl-2降低,而caspase-3和BAX的表达较高。
■EPO可以有效提高LIRI，这可能与FGF23/FGFR4/p-ERK1/2信号通路的激活有关。
