Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Apr;69(4):365-373.
doi: 10.1007/s00011-020-01331-3. Epub 2020 Mar 4.

Emodin alleviated pulmonary inflammation in rats with LPS-induced acute lung injury through inhibiting the mTOR/HIF-1α/VEGF signaling pathway

Xiaoqian Li  1   2 , Cong Shan  1   2 , Zhonghua Wu  1   2 , Hongji Yu  1   2 , Aidong Yang  3   4 , Bo Tan  5
Affiliations

Emodin alleviated pulmonary inflammation in rats with LPS-induced acute lung injury through inhibiting the mTOR/HIF-1α/VEGF signaling pathway

Xiaoqian Li et al. Inflamm Res. 2020 Apr.

Erratum in

Abstract

Objective and design: This study aimed to investigate the anti-pulmonary inflammation effect of emodin on Wistar rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI) and RAW264.7 cells through the mammalian target of rapamycin (mTOR)/hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway.

Subjects: Wistar rats and RAW264.7 cells were studied.

Treatment: LPS was used to induce inflammation in rats or RAW264.7 cells and emodin was given once a day before LPS stimulation and continued for a certain number of days.

Methods: Lung tissues and bronchoalveolar lavage fluid (BALF) were collected for the in vivo experiment, while cells and supernatant were collected for the in vitro experiment. Pathological changes in the lung tissues were assessed by hematoxylin and eosin staining. The levels of inflammatory factors, including TNF-α, IL-1β, and IL-6, were determined by enzyme-linked immunosorbent assay. The expression levels of p-mTOR, HIF-1α, and VEGF proteins were measured by Western blot analysis and immunohistochemistry. The mRNA levels of p70S6K, eIF4E-BP1, and eIF4E were measured by quantitative polymerase chain reaction.

Results: Emodin ameliorated pathological changes and infiltrated inflammatory cells in LPS-induced ALI. It also significantly reduced the expression of inflammatory factors, including TNF-α, IL-1β, and IL-6, in BALF and downregulated the expression of p-mTOR, HIF-1α, and VEGF proteins in the lung tissues. Similar anti-inflammatory effects and the downregulation of the mTOR/HIF-1α/VEGF signaling pathway were found in RAW264.7 cells. The mRNA levels of p70S6K, eIF4E-BP1, and eIF4E also decreased in the macrophages.

Conclusion: Emodin alleviated LPS-induced pulmonary inflammation in rat lung tissues and RAW264.7 cells through inhibiting the mTOR/HIF-1α/VEGF signaling pathway, which accounted for the therapeutic effects of emodin on ALI.

Keywords: Acute lung injury; Emodin; Pulmonary inflammation; mTOR/HIF-1α/VEGF signaling pathway.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Annu Rev Physiol. 2014;76:467-92 - PubMed
    1. Int Immunopharmacol. 2016 May;34:16-24 - PubMed
    1. J Tradit Chin Med. 2001 Mar;21(1):54-8 - PubMed
    1. Mol Med Rep. 2017 Oct;16(4):5121-5128 - PubMed
    1. Am J Physiol Lung Cell Mol Physiol. 2002 Sep;283(3):L585-95 - PubMed

MeSH terms

LinkOut - more resources