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Dihydrokaempferol attenuates LPS-induced inflammation and apoptosis in WI-38 cellsQiao
Wang, Qiao; Zhang, Liwen; Pang, Ping.
Afiliação
  • Wang, Qiao; Guizhou University of Traditional Chinese Medicine. The Second Affiliated Hospital. Department of Pediatrics. Guiyang. China
  • Zhang, Liwen; Guizhou University of Traditional Chinese Medicine. The Second Affiliated Hospital. Department of Pediatrics. Guiyang. China
  • Pang, Ping; Guizhou University of Traditional Chinese Medicine. The Second Affiliated Hospital. Department of Pediatrics. Guiyang. China
Allergol. immunopatol ; 51(6): 23-29, 2023. graf
Article em En | IBECS | ID: ibc-227305
Biblioteca responsável: ES1.1
Localização: ES15.1 - BNCS
ABSTRACT
Background: Globally, pneumonia has been associated as a primary cause of mortality in children aged less than 5 years. Dihydrokaempferol (DHK) has been proposed for being correlated with the process of various diseases. Nevertheless, whether DHK has a role in the progression of infantile pneumonia remains unclear. This study aimed at exploring whether DHK was involved in the progression of infantile pneumonia. Methods: Human fibroblast cells WI-38 were treated with lipopolysaccharide (LPS). The viability of WI-38 cells was measured via Cell counting kit-8. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). Western blot analysis revealed the protein levels of IL-1β, IL-6, TNF-α, Bax, and cleaved-caspase 3. Flow cytometry was applied for exploring the apoptosis of WI-38 cells. The concentrations of IL-1β, IL-6, and TNF-α were assessed via enzyme-linked-immunosorbent serologic assay. Results: DHK modulated the viability of WI-38 cells in infantile pneumonia. Furthermore, we identified that DHK treatment inversely changed LPS induction-mediated elevation on the levels of inflammation biomarkers. Besides, DHK counteracted LPS-induced production of reactive oxygen species (ROS) in WI-38 cells. DHK also decreased LPS-induced elevation of WI-38 cells apoptosis and mediated the levels of apoptosis-associated indexes. Moreover, modulating sirtuin-1 (SIRT1) protein level was lowered by the induction of LPS, and was reversed by DHK treatment. In addition, DHK counteracted LPS induction-mediated elevation of p-p65 and phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha (p-IκBα) protein levels. Conclusion: DHK alleviated LPS-induced WI-38 cells inflammation injury in infantile pneumonia through SIRT1/NF-κB pathway. The results shed light on the implications of DHK on the prevention and treatment of infantile pneumonia (AU)
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Texto completo: 1 Coleções: 06-national / ES Base de dados: IBECS Assunto principal: Pneumonia / Lipopolissacarídeos / Apoptose Limite: Child / Humans Idioma: En Revista: Allergol. immunopatol Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 06-national / ES Base de dados: IBECS Assunto principal: Pneumonia / Lipopolissacarídeos / Apoptose Limite: Child / Humans Idioma: En Revista: Allergol. immunopatol Ano de publicação: 2023 Tipo de documento: Article