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Coptisine attenuates sepsis lung injury by suppressing LPS-induced lung epithelial cell inflammation and apoptosis
Huang, Junjun; Ren, Ke; Huang, Lili.
Afiliação
  • Huang, Junjun; Nantong University. Affiliated Nantong Third Hospital. Department of Intensive Care Unit. Nantong. China
  • Ren, Ke; Nantong University. Affiliated Nantong Third Hospital. Department of Intensive Care Unit. Nantong. China
  • Huang, Lili; Nantong University. Affiliated Nantong Third Hospital. Department of Respiratory Medicine. Nantong. China
Allergol. immunopatol ; 51(6): 30-36, 2023. graf
Artigo em Inglês | IBECS | ID: ibc-227306
Biblioteca responsável: ES1.1
Localização: ES15.1 - BNCS
ABSTRACT

Objective:

This study aimed to investigate the functioning and mechanism of coptisine in acute lung injury (ALI).

Methods:

Murine Lung Epithelial 12 (MLE-12) cells were stimulated with lipopolysaccharide (LPS) to construct an in vitro pulmonary injury model to study the functioning of coptisine in sepsis-induced ALI. The viability of MLE-12 cells was assessed by the cell counting kit-8 assay. The cytokine release of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and IL-1β was measured by enzyme-linked-immunosorbent serologic assay. The relative expression levels of TNF-α, IL-6, and IL-1β mRNA were examined by reverse transcription-quantitative polymerase chain reaction. The cell apoptosis of MLE-12 cells was determined by Annexin V/propidium iodide staining and analyzed by flow cytometry. The expressions of apoptosis-related proteins Bax and cleaved Caspase-3 were observed by Western blot analysis. The activation of nuclear factor kappa B (NF-κB) signaling pathway was discovered by the determination of phospho-p65, p65, phospho-nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα), and IκBα through Western blot analysis.

Results:

Coptisine treatment could significantly restore decrease in MLE-12 cell viability caused by LPS stimulation. The release of TNF-α, IL-6, and IL-1β was significantly inhibited by coptisine treatment. Coptisine treatment inhibited MLE-12 cell apoptosis induced by LPS, and also inhibited the expression levels of Bax and cleaved Caspase-3. Coptisine treatment along with LPS stimulation, significantly reduced the protein level of phospho-IκBα, increased the level of IκBα, and reduced phospho-p65–p65 ratio.

Conclusion:

These results indicated that coptisine attenuated sepsis lung injury by suppressing lung epithelial cell inflammation and apoptosis through NF-κB pathway. Therefore, coptisine may have potential to treat sepsis-induced ALI (AU)
Assuntos


Texto completo: Disponível Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Pneumonia / Lesão Pulmonar Aguda Limite: Animais / Humanos Idioma: Inglês Revista: Allergol. immunopatol Ano de publicação: 2023 Tipo de documento: Artigo Instituição/País de afiliação: Nantong University/China

Texto completo: Disponível Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Pneumonia / Lesão Pulmonar Aguda Limite: Animais / Humanos Idioma: Inglês Revista: Allergol. immunopatol Ano de publicação: 2023 Tipo de documento: Artigo Instituição/País de afiliação: Nantong University/China
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