Suppression of sirtuin 1 alleviates airway inflammation through mTOR‑mediated autophagy
- Yuanyuan Wu
- Wei Li
- Yifan Hu
- Yun Liu
- Xiuzhen Sun
Affiliations: Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China
- Published online on: July 13, 2020 https://doi.org/10.3892/mmr.2020.11338
Copyright: © Wu
et al. This is an open access article distributed under the
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Sirtuin 1 (SIRT1) is involved in the pathogenesis of allergic asthma. This study aimed to investigate whether EX‑527, a specific SIRT1 inhibitor, exerted suppressive effects on allergic airway inflammation in mice submitted to ovalbumin (OVA) inhalation. In addition, this study assessed whether such a protective role was mediated by autophagy suppression though mammalian target of rapamycin (mTOR) activation. Female C57BL/6 mice were sensitized to OVA and EX‑527 (10 mg/kg) was administered prior to OVA challenge. The study found that EX‑527 reversed OVA‑induced airway inflammation, and reduced OVA‑induced increases in inflammatory cytokine expression, and total cell and eosinophil counts in bronchoalveolar lavage fluid. In addition, EX‑527 enhanced mTOR activation, thereby suppressing autophagy in allergic mice. To assess whether EX‑527 inhibited airway inflammation in asthma through the mTOR‑mediated autophagy pathway, rapamycin was administered to mice treated with EX‑527 after OVA sensitization. All effects induced by EX‑527, including increased phosphorylated‑mTOR and decreased autophagy, were abrogated by rapamycin treatment. Taken together, the present findings indicated that EX‑527 may inhibit allergic airway inflammation by suppressing autophagy, an effect mediated by mTOR activation in allergic mice.