Erythromycin Attenuates Hyperoxia Induced Lung Injury by Enhancing GSH Expression and Inhibiting Expression of Inflammatory Cytokines.

IF 0.7 4区 医学 Q4 PATHOLOGY
Fetal and Pediatric Pathology Pub Date : 2023-10-01 Epub Date: 2023-06-21 DOI:10.1080/15513815.2023.2223722
Xiaoyun Chu, Xiaoyue Zhang, Bowen Weng, Xiaotong Yin, Cheng Cai
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引用次数: 0

Abstract

Introduction: Oxidative stress and inflammation have proven to be key factors contributing to the occurrence of BPD. Erythromycin has been shown to be effective in treating the redox imbalance seen in many non-bacterial infectious chronic inflammatory diseases. Methods: Ninety-six premature rats were randomly divided into air + saline chloride group, air + erythromycin group, hyperoxia + saline chloride group and hyperoxia + erythromycin group. Lung tissue specimens were collected from 8 premature rats in each group on days 1, 7 and 14, respectively. Results: Pulmonary pathological changes in premature rats after hyperoxia exposure were similar to those of BPD. Hyperoxia exposure induced high expression of GSH, TNF-α, and IL-1β. Erythromycin intervention caused a further increase in GSH expression and a decrease in TNF-α and IL-1β expression. Conclusion: GSH, TNF-α and IL-1β are all involved in the development of BPD. Erythromycin may alleviate BPD by enhancing the expression of GSH and inhibiting the release of inflammatory mediators.

红霉素通过增强GSH的表达和抑制炎症细胞因子的表达来减轻高氧诱导的肺损伤。
引言:氧化应激和炎症已被证明是导致BPD发生的关键因素。红霉素已被证明能有效治疗许多非细菌感染性慢性炎症疾病中的氧化还原失衡。方法:将96只早产大鼠随机分为空气组 + 氯化盐水组,空气 + 红霉素组,高氧 + 氯化盐水组与高氧 + 红霉素组。分别在第1天、第7天和第14天从每组8只早产大鼠身上采集肺组织标本。结果:早产大鼠高氧暴露后的肺部病理变化与BPD相似。高氧暴露诱导GSH、TNF-α和IL-1β的高表达。红霉素干预导致GSH表达进一步增加,TNF-α和IL-1β表达降低。结论:GSH、TNF-α和IL-1β均参与BPD的发生发展。红霉素可通过增强GSH的表达和抑制炎症介质的释放来减轻BPD。
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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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