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Peer-reviewedCC BY-NC-NDJournal of cardiothoracic surgery

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

  • Wencai Wang1
  • Wenhao Wang2
  • Xingchen Liu3
  • Woda Shi4
4 affiliations
  1. 1Department of Cardiothoracic Surgery, Yancheng Third People's Hospital, The affiliated hospital of Jiangsu Vocational College of Medicine, Yancheng, 224000, Jiangsu, China.
  2. 2Department of thoracic surgery, The First Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China.
  3. 3Department of Cardiothoracic Surgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, No.75 Juchang Road, Yancheng, 224000, Jiangsu, China.
  4. 4Department of Cardiothoracic Surgery, Affiliated Hospital 6 of Nantong University, Yancheng Third People's Hospital, No.75 Juchang Road, Yancheng, 224000, Jiangsu, China. [email protected].
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{wang2026mogroside,
  title = {{Mogroside V regulates autophagy through AMPK/mTOR pathway to ameliorate cigarette smoke-induced acute lung injury.}},
  author = {Wencai Wang and Wenhao Wang and Xingchen Liu and Woda Shi},
  journal = {Journal of cardiothoracic surgery},
  year = {2026},
  month = aug,
  doi = {10.1186/s13019-026-04556-1},
  url = {https://europepmc.org/article/MED/42958396},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Mogroside V regulates autophagy through AMPK/mTOR pathway to ameliorate cigarette smoke-induced acute lung injury.
AU  - Wencai Wang
AU  - Wenhao Wang
AU  - Xingchen Liu
AU  - Woda Shi
PY  - 2026
DA  - 2026/08/01
JO  - Journal of cardiothoracic surgery
DO  - 10.1186/s13019-026-04556-1
UR  - https://europepmc.org/article/MED/42958396
AB  - 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.
SN  - 1749-8090
ER  -