Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 96, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2021.107621
Keywords
Platycodin D; Lipopolysaccharide; Acute lung injury; NLRP3; TLR4/MyD88/NF-kappa B
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Funding
- Department of Science and Technology of Sichuan Province, Key RD Programme [2020YFS0312]
- Miaozi Innovation Program for Science and technology of Sichuan Province [2019055]
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Pre-treatment with PLD alleviates lung inflammation and injury induced by LPS, reduces inflammatory cytokine levels, modulates oxidative stress-related factors in lung tissue, and inhibits the activation of NLRP3 and NF-kappa B signaling pathway.
Acute lung injury (ALI) is a common clinical condition with a high mortality rate and no specific treatment is available. An excessive inflammatory response contributes to the development of ALI and accelerates its progression, and the NLRP3 inflammasome and NF-kappa B signaling pathways are key players in inflammation. Platycodin D has been reported to have anti-oxidant and anti-stress properties in various diseases. However, the effects of PLD in ALI has not been clearly demonstrated. The aim of this study was to investigate the therapeutic effects of PLD on ALI and its possible mechanism. Our study found that PLD pre-treatment attenuated lung histopathological injury in LPS-induced SD rats and reduced the levels of inflammatory cytokines and lung wet/dry ratio in bronchoalveolar lavage fluid (BALF). In addition, PLD modulate LPS-induced production of MDA, MPO, GSH, GSH-Px and CAT in lung tissue. In addition, PLD suppressed the activation of NLRP3 inflammatory microsomes and the NF-kappa B signaling pathway. Thus, our results suggest that PLD are protective against LPS-induced ALI by inhibiting NLRP3 and NF-kappa B signaling pathway.
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