FDP对呼吸窘迫综合征大鼠肺组织氧化应激及PKR水平的影响  

Effects of FDP on oxidative stress and PKR levels in lung tissues of rats with respiratory distress syndrome

作　　者：谢勇杰 江叶舟 彭瑶 钟燕军 XIE Yong-jie;JIANG Ye-zhou;PENG Yao;ZHONG Yan-jun(General outpatient Department,Hunan Thoracic Hospital,Changsha 410006;Critical Care Department,Xiangya Hospital,Central South University,Changsha 410013,China)

机构地区：[1]湖南省胸科医院综合门诊部,湖南长沙410006 [2]中南大学湘雅医院重症科,湖南长沙410013

出　　处：《解剖科学进展》2023年第4期363-366,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金项目(81701962)。

摘　　要：目的探讨不同浓度FDP(1,6-二磷酸果糖)对呼吸窘迫综合征(ARDS)大鼠肺组织氧化应激水平及PKR信号通路的影响。方法40只SPF级SD大鼠随机分为正常组、ARDS组及低干预组、中干预组及高干预组,每组8只。苏木素伊红(HE)染色观察肺组织病理改变;ELISA检测肺组织氧化应激指标;TUNEL法检测肺组织细胞凋亡;免疫印迹及RT-PCR分别检测肺组织PKR和NF-κB的表达水平。结果与ARDS组相比,低、中及高干预组大鼠炎症浸润降低,纤维断裂改善;大鼠肺组织HYP、MDA、TNF-α及IL-1β水平降低,SOD及GSH-Px水平升高(P<0.05);肺组织细胞凋亡率降低(P<0.05);肺组织中PKR及NF-κB的蛋白及mRNA含量均降低(P<0.05),且高干预组最为显著。结论1,6-二磷酸果糖可能通过抑制PKR及NF-κB信号通路抑制呼吸窘迫综合征大鼠氧化应激与肺细胞凋亡。Objective To investigate the effects of different concentrations of FDP(fructose 1,6-diphosphate)on oxidative stress level and PKR signaling pathway in lung tissue of rats with respiratory distress syndrome(ARDS).Methods Forty SPF SD rats were randomly divided into normal group,ARDS group,low intervention group,medium intervention group and high intervention group,with 8 rats in each group.The pathological changes of lung tissue were observed by hematoxylin eosin(HE)staining.The oxidative stress index of lung tissue was detected by ELISA.Apoptosis of cells in lung was detected by TUNEL method.The expressions of PKR and NF-κB in lung tissues were detected by western blot and RTPCR.Results Compared with ARDS group,inflammatory infiltration was decreased and fiber breakage was improved in lung tissues of rats in low,medium and high intervention groups.The levels of HYP,MDA,TNF-αand IL-1βin lung tissues were decreased,while the levels of SOD and GSH-Px were increased(P<0.05).The apoptosis rate of cells in lung tissue was decreased(P<0.05).The contents of PKR and NF-κB protein and mRNA in lung tissues were decreased(P<0.05),and the high intervention group was the most significant(P<0.05).Conclusion Fructose 1,6-diphosphate may inhibit oxidative stress and apoptosis of cells in lung of rats with respiratory distress syndrome by inhibiting PKR and NF-κB signaling pathways.

关 键 词：呼吸窘迫综合征 1 6-二磷酸果糖 氧化应激 肺细胞凋亡 

分 类 号：R563.8[医药卫生—呼吸系统]