Shikonin ameliorates injury and inflammatory response of LPS-stimulated WI-38 cells via modulating the miR-489-3p/MAP2K1 axis.

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Tytuł:: Shikonin ameliorates injury and inflammatory response of LPS-stimulated WI-38 cells via modulating the miR-489-3p/MAP2K1 axis.
Autorzy:: Wang J; Department of Pharmacy, Jiangsu Health vocational college, Nanjing 211800, Jiangsu, China.
Chen Z; Department of Outpatient, Jurong People's Hospital, Zhenjiang 212400, Jiangsu, China.
Feng X; Department of Comprehensive ICU, Luoyang Central Hospital, Luoyang 471009, Henan, China.
Yin L; Department of Comprehensive ICU, Luoyang Central Hospital, Luoyang 471009, Henan, China.
Źródło:: Environmental toxicology [Environ Toxicol] 2021 Sep; Vol. 36 (9), pp. 1775-1784. Date of Electronic Publication: 2021 Jun 05.
Typ publikacji:: Journal Article
Język:: English
Imprint Name(s):: Original Publication: New York, NY : John Wiley & Sons, c1999-
MeSH Terms:: MicroRNAs*/genetics
Naphthoquinones*/pharmacology
Apoptosis ; Lipopolysaccharides/toxicity
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Contributed Indexing:: Keywords: MAP2K1; MAPK pathway; miR-489-3p; pneumonia
Substance Nomenclature:: 0 (Lipopolysaccharides)
0 (MicroRNAs)
0 (Naphthoquinones)
3IK6592UBW (shikonin)
Entry Date(s):: Date Created: 20210605 Date Completed: 20210812 Latest Revision: 20210812
Update Code:: 20240105
DOI:: 10.1002/tox.23298
PMID:: 34089293
: Czasopismo naukowe

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Pneumonia is an inflammatory disease induced by infection with different pathogens. Currently, multiple preclinical studies have revealed that shikonin, a natural naphthoquinone, can mitigate lipopolysaccharide (LPS)-induced inflammation, but its underlying mechanism in pneumonia remains unknown. This research was designed to explore the function and regulatory mechanism of shikonin in LPS-induced cell injury and inflammation in WI-38 cells. In-vitro model of pneumonia was constructed by treating WI-38 cells with LPS. Expression of miR-489-3p and MAP2K1 was tested by RT-qPCR and (or) Western blot analysis. Cell viability was examined by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay. The productions of pro-inflammatory cytokines were determined by enzyme-linked immunosorbent assays. Cell apoptosis was detected by Western blot and flow cytometry analysis. In the current study, LPS induced WI-38 cell damage by inhibiting cell viability and promoting cell apoptosis and inflammation. Shikonin ameliorated LPS-induced cell injury and elevated miR-489-3p expression. LPS-induced inflammatory injury was further mitigated by upregulation of miR-489-3p. In addition, MAP2K1, the target of miR-489-3p, was upregulated by LPS. Furthermore, upregulation of MAP2K1 reversed the influence of shikonin and miR-489-3p mimics on LPS-induced cell injury and inflammation. This study revealed that shikonin protected WI-38 cells against LPS-induced cell injury and inflammatory response by regulating the miR-489-3p/MAP2K1 axis, thus affecting the progression of pneumonia.
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