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Background <p>Cigarette smoke causes acute lung injury (ALI). Mogroside V (MV) has been recently found to relieve cough and asthma symptoms and to eliminate phlegm. We tested the potential and mechanism of action of MV in alleviating cigarette smoke-induced ALI.</p> Methods <p>We explored the effects and mechanisms of action of MV by using cigarette smoke extracts (CSE) in lung‑on‑a‑chip and mouse models. The levels of IL-18, IL-1β and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA) and qRT-PCR. Pulmonary gas-blood barrier was detected by qRT-PCR and western blot. TEER and FITC-dextran permeability assay measured cell barrier function. Western blot and qRT-PCR were used to detect the expression of autophagy-related genes and AMPK/mTOR signaling pathway-related proteins.</p> Results <p>CSE treatment caused an increase in inflammatory factors in a lung‑on‑a‑chip model. After MV treatment, the expression of pro-inflammatory factors decreased, the pulmonary gas-blood barrier disruption was improved in response to CSE. MV promoted autophagy and regulated the AMPK/mTOR pathway.</p> Conclusion <p>MV promotes autophagy and ameliorates cigarette smoke-induced ALI through the AMPK/mTOR signaling pathway in vitro and in vivo.</p>

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Mogroside V regulates autophagy through AMPK/mTOR pathway to ameliorate cigarette smoke-induced acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月1日

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  • Wencai Wang,
  • Wenhao Wang,
  • Xingchen Liu,
  • Woda Shi

摘要

Background

Cigarette smoke causes acute lung injury (ALI). Mogroside V (MV) has been recently found to relieve cough and asthma symptoms and to eliminate phlegm. We tested the potential and mechanism of action of MV in alleviating cigarette smoke-induced ALI.

Methods

We explored the effects and mechanisms of action of MV by using cigarette smoke extracts (CSE) in lung‑on‑a‑chip and mouse models. The levels of IL-18, IL-1β and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA) and qRT-PCR. Pulmonary gas-blood barrier was detected by qRT-PCR and western blot. TEER and FITC-dextran permeability assay measured cell barrier function. Western blot and qRT-PCR were used to detect the expression of autophagy-related genes and AMPK/mTOR signaling pathway-related proteins.

Results

CSE treatment caused an increase in inflammatory factors in a lung‑on‑a‑chip model. After MV treatment, the expression of pro-inflammatory factors decreased, the pulmonary gas-blood barrier disruption was improved in response to CSE. MV promoted autophagy and regulated the AMPK/mTOR pathway.

Conclusion

MV promotes autophagy and ameliorates cigarette smoke-induced ALI through the AMPK/mTOR signaling pathway in vitro and in vivo.