Abstract | BACKGROUND: METHODS: Cell viability was examined by CCK-8 assay. The relative expression of miR-132-3p, FOXO3 were detected by qPCR. The levels of TNF-α, IL-6 and IL-1β were detected using enzyme-linked immunosorbent assay. The amount of apoptosis cells was detected by flow cytometry. The protein levels of Bcl-2, Bax, p-p65 and p-IκBα were measured by western blot. RESULTS: We found that DHQ-induced the expression of miR-132-3p in LPS-induced ALI. Overexpression of miR-132-3p resulted in the inhibition of FOXO3 expression and then suppressed FOXO3-activated NF-κB pathway, attenuating LPS-induced inflammatory response and apoptosis. CONCLUSION: We demonstrated FOXO3 to be a target of miR-132-3p, and DHQ could induce the expression of miR-132-3p, relieving LPS-induced ALI via miR-132-3p/FOXO3/NF-κB axis, providing a promising therapeutic target for ALI.
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Authors | Jian-Hua Liu, Liang Cao, Chang-Hong Zhang, Chen Li, Zhi-Hua Zhang, Qi Wu |
Journal | Pulmonary pharmacology & therapeutics
(Pulm Pharmacol Ther)
Vol. 64
Pg. 101934
(10 2020)
ISSN: 1522-9629 [Electronic] England |
PMID | 32805387
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2020 Elsevier Ltd. All rights reserved. |
Chemical References |
- FOXO3 protein, human
- Forkhead Box Protein O3
- Lipopolysaccharides
- MIRN132 microRNA, human
- MicroRNAs
- NF-kappa B
- Quercetin
- taxifolin
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Topics |
- Acute Lung Injury
(chemically induced, drug therapy)
- Forkhead Box Protein O3
(genetics)
- Humans
- Lipopolysaccharides
(toxicity)
- MicroRNAs
(genetics)
- NF-kappa B
- Quercetin
(analogs & derivatives)
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