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Knocking down TNFAIP1 alleviates inflammation and oxidative stress in pediatric pneumonia through PI3K/Akt/Nrf2 pathway
Chen, Jing; Zhao, Mengtian; Fang, Wei; Du, Chaojun.
Affiliation
  • Chen, Jing; Anhui Provincial Children's Hospital. Department of Pediatric Cardiovascular Surgery. Hefei. China
  • Zhao, Mengtian; Anhui Provincial Children's Hospital. Department of Neonatal Surgery. Hefei. China
  • Fang, Wei; Anhui Provincial Children's Hospital. Department of Pediatric Cardiovascular Surgery. Hefei. China
  • Du, Chaojun; Anhui Provincial Children's Hospital. Department of Pediatric Cardiovascular Surgery. Hefei. China
Allergol. immunopatol ; 51(4): 94-100, 2023. graf, ilus
Article in English | IBECS | ID: ibc-222639
Responsible library: ES1.1
Localization: ES15.1 - BNCS
ABSTRACT

Background:

Pneumonia is an acute respiratory infection with increasing global incidences. Children are more susceptible to pneumonia than adults, and its incidences grow extremely high during peak seasons. Thus, it is necessary to investigate the pathogenesis and molecular mechanism of childhood pneumonia.

Methods:

This study examined the role of tumor necrosis factor alpha-inducible protein 1 (TNFAIP1) in lipopolysaccharide (LPS)-induced pneumonia mice. After LPS exposure, lung function, TNFAIP1 activation, infarction volume, oxidative stress, lung tissue apoptosis ratio, and inflammatory response were assessed by immunohistochemistry staining, hematoxylin and eosin staning, Western blot analysis, terminal deoxynucleotidyl transferase dUTP nick end labelling assay, and enzyme-linked-immunosorbent serologic assay, respectively. The mechanism of TNFAIP1 regulating phosphoinositide 3-kinases (PI3K)–protein kinase B (Akt)–nuclear factor erythroid 2-related factor 2 (Nrf2) pathway was analyzed by Western blot analysis.

Results:

TNFAIP1 expression was enhanced in the LPS-induced pneumonia mice but was negatively correlated with the LPS-induced lung injury. Silencing TNFAIP1 alleviated inflammatory response, production of reactive oxygen species (ROS), and cellular apoptosis in LPS-induced pneumonia. Moreover, PI3K/Akt/Nrf2 signaling pathways were predominantly involved in the TNFAIP1-mediated lung injury, which also played a role in the process of LPS-induced pneumonia.

Conclusion:

This study suggested that TNFAIP1 acted as a negative regulator of acute pneumonia by attenuating inflammatory response, production of ROS, and cellular apoptosis via PI3K/Akt/Nrf2 pathway. The findings suggested that TNFAIP1 is a potential candidate for pneumonia therap (AU)
Subject(s)

Full text: Available Collection: National databases / Spain Database: IBECS Main subject: Pneumonia / Oxidative Stress / Adaptor Proteins, Signal Transducing / Proto-Oncogene Proteins c-akt / NF-E2-Related Factor 2 Limits: Animals Language: English Journal: Allergol. immunopatol Year: 2023 Document type: Article Institution/Affiliation country: Anhui Provincial Children's Hospital/China
Full text: Available Collection: National databases / Spain Database: IBECS Main subject: Pneumonia / Oxidative Stress / Adaptor Proteins, Signal Transducing / Proto-Oncogene Proteins c-akt / NF-E2-Related Factor 2 Limits: Animals Language: English Journal: Allergol. immunopatol Year: 2023 Document type: Article Institution/Affiliation country: Anhui Provincial Children's Hospital/China
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