期刊
INFLAMMATION RESEARCH
卷 69, 期 4, 页码 365-373出版社
SPRINGER BASEL AG
DOI: 10.1007/s00011-020-01331-3
关键词
Acute lung injury; Emodin; mTOR; HIF-1 alpha; VEGF signaling pathway; Pulmonary inflammation
资金
- Ministry of Science and Technology of the People's Republic of China [2018YFC1704100, 2017ZX09304002] Funding Source: Medline
- National Natural Science Foundation of China [81673855] Funding Source: Medline
- Shanghai Municipal Commission (CN) [ZY(2018-2020)-CCCX-2001-01] Funding Source: Medline
- Shanghai University of Traditional Chinese Medicine (CN) [A1-Z193020109] Funding Source: Medline
- Shanghai Municipal Commission of Economy and Informatization (CN) [201740199] Funding Source: Medline
- Shanghai Shuguang Hospital (CN) [SGXZ-201907] Funding Source: Medline
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-1 alpha (HIF-1 alpha)/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-alpha, IL-1 beta, and IL-6, were determined by enzyme-linked immunosorbent assay. The expression levels of p-mTOR, HIF-1 alpha, 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-alpha, IL-1 beta, and IL-6, in BALF and downregulated the expression of p-mTOR, HIF-1 alpha, and VEGF proteins in the lung tissues. Similar anti-inflammatory effects and the downregulation of the mTOR/HIF-1 alpha/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-1 alpha/VEGF signaling pathway, which accounted for the therapeutic effects of emodin on ALI.
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