Stachyose attenuates IL-33-associated pulmonary inflammation and GPX4-related redox imbalance in MPTP-treated mice
- 1Institute of Geriatrics, the 2nd Medical Center, Beijing Key Laboratory of Aging and Geriatrics, National Clinical Research Center for Geriatrics Diseases, Chinese PLA General Hospital, 28 Fuxing Road, Beijing, 100853, China
- 2Corresponding author.
Abstract
Background: Parkinson's disease (PD) involves central neurodegeneration and peripheral dysfunction. Whether interleukin-33 (IL-33)-associated airway inflammatory stress modifies intestinal, pulmonary, and nigrostriatal abnormalities in mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and whether stachyose (STA) attenuates them, remains unclear. Methods: C57BL/6 J mice were assigned to control (Ctrl), Ctrl + IL-33, PD, PD + IL-33, or PD + IL-33 + STA groups. MPTP induced PD-like injury; IL-33 was administered intranasally and STA orally. Behavioral, histological, inflammatory, dopaminergic, tight-junction-associated, and pulmonary glutathione peroxidase 4 (GPX4)-related redox and iron indices were assessed. STA–GPX4 compatibility was explored by docking and 100-ns molecular dynamics simulation. Results: MPTP impaired behavior, increased midbrain α-synuclein (α-syn), and reduced tyrosine hydroxylase (TH). IL-33 alone induced pulmonary inflammation without reproducing the parkinsonian phenotype. On the MPTP-treated background, IL-33 increased lung injury, pro-inflammatory cytokines, and ferrous iron while reducing interleukin-10 (IL-10), GPX4, and the ratio of reduced glutathione to oxidized glutathione (GSH/GSSG). Compared with PD + IL-33 mice, STA improved behavior, attenuated colonic and pulmonary injury and cytokine imbalance, partially restored tight-junction-associated transcripts, reduced α-syn, restored TH and GPX4, improved GSH/GSSG, and lowered ferrous iron. Computational analyses predicted polar interactions involving lysine 127 and arginine 152 and supported stability of the complex in silico. Conclusion: Compared with Ctrl + IL-33 mice, PD + IL-33 mice showed greater pulmonary inflammation and GPX4-related redox and iron disturbances. STA partially alleviated abnormalities under the combined challenge. These findings do not establish causal inter-organ communication, ferroptotic cell death, microbiota dependence, or direct STA–GPX4 target engagement.
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BibTeX
@article{wei2026stachyose,
title = {{Stachyose attenuates IL-33-associated pulmonary inflammation and GPX4-related redox imbalance in MPTP-treated mice}},
author = {Meng Wei and Heran Wang and Yazhuo Hu and Ya Qiu and Jianjun Jia},
journal = {Allergy Medicine},
year = {2026},
month = oct,
doi = {10.1016/j.allmed.2026.100132},
url = {https://doi.org/10.1016/j.allmed.2026.100132},
note = {CC BY},
}
RIS
TY - JOUR
TI - Stachyose attenuates IL-33-associated pulmonary inflammation and GPX4-related redox imbalance in MPTP-treated mice
AU - Meng Wei
AU - Heran Wang
AU - Yazhuo Hu
AU - Ya Qiu
AU - Jianjun Jia
PY - 2026
DA - 2026/10/30
JO - Allergy Medicine
DO - 10.1016/j.allmed.2026.100132
UR - https://doi.org/10.1016/j.allmed.2026.100132
AB - Background: Parkinson's disease (PD) involves central neurodegeneration and peripheral dysfunction. Whether interleukin-33 (IL-33)-associated airway inflammatory stress modifies intestinal, pulmonary, and nigrostriatal abnormalities in mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and whether stachyose (STA) attenuates them, remains unclear. Methods: C57BL/6 J mice were assigned to control (Ctrl), Ctrl + IL-33, PD, PD + IL-33, or PD + IL-33 + STA groups. MPTP induced PD-like injury; IL-33 was administered intranasally and STA orally. Behavioral, histological, inflammatory, dopaminergic, tight-junction-associated, and pulmonary glutathione peroxidase 4 (GPX4)-related redox and iron indices were assessed. STA–GPX4 compatibility was explored by docking and 100-ns molecular dynamics simulation. Results: MPTP impaired behavior, increased midbrain α-synuclein (α-syn), and reduced tyrosine hydroxylase (TH). IL-33 alone induced pulmonary inflammation without reproducing the parkinsonian phenotype. On the MPTP-treated background, IL-33 increased lung injury, pro-inflammatory cytokines, and ferrous iron while reducing interleukin-10 (IL-10), GPX4, and the ratio of reduced glutathione to oxidized glutathione (GSH/GSSG). Compared with PD + IL-33 mice, STA improved behavior, attenuated colonic and pulmonary injury and cytokine imbalance, partially restored tight-junction-associated transcripts, reduced α-syn, restored TH and GPX4, improved GSH/GSSG, and lowered ferrous iron. Computational analyses predicted polar interactions involving lysine 127 and arginine 152 and supported stability of the complex in silico. Conclusion: Compared with Ctrl + IL-33 mice, PD + IL-33 mice showed greater pulmonary inflammation and GPX4-related redox and iron disturbances. STA partially alleviated abnormalities under the combined challenge. These findings do not establish causal inter-organ communication, ferroptotic cell death, microbiota dependence, or direct STA–GPX4 target engagement.
SN - 2949-9135
ER -