Spermidine Prevents Polarity Loss of Absorptive Enterocytes in Jejunum of Lipopolysaccharide-Challenged Mice via 4D-DIA Proteomics Analysis

Spermidine Prevents Polarity Loss of Absorptive Enterocytes in Jejunum of Lipopolysaccharide-Challenged Mice via 4D-DIA Proteomics Analysis

Identifying effective compounds to restore the polarity of absorptive enterocytes (AEs) holds promise for mitigating the severity and duration of small intestinal disorders. Spermidine (SPD) is a natural polyamine; whether it can repair inflammation-induced loss of AE polarity remains unclear. In th...

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主要作者: Pengchao Zheng (22674589) (author)
其他作者: Shiyi Tian (5868122) (author), Zhen Chen (129176) (author), Yi Zhang (9093) (author), Keyi Jiang (3603341) (author), Ziyang Zha (22674592) (author), Jue Wang (58890) (author), Baosheng Liu (3042366) (author)
出版: 2025
主题:
Biochemistry
Physiology
Immunology
Astronomical and Space Sciences not elsewhere classified
Chemical Sciences not elsewhere classified
small intestinal disorders
proteomic analysis revealed
apical slc transporters
2 cell model
specific immune responses
spd supplementation enhanced
spd effectively alleviates
spd attenuated mucosal
inflammatory responses
treated mice
significantly downregulating
results demonstrated
proteins involved
protein groups
pards ),
natural polyamine
inflammatory effect
induced loss
independent acquisition
holds promise
hdac4 signaling
findings indicate
epithelial morphology
cytoskeletal proteins
crypt ratio
challenged mice
antioxidant capacity
absorptive enterocytes
4d data
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总结:Identifying effective compounds to restore the polarity of absorptive enterocytes (AEs) holds promise for mitigating the severity and duration of small intestinal disorders. Spermidine (SPD) is a natural polyamine; whether it can repair inflammation-induced loss of AE polarity remains unclear. In this study, we employed lipopolysaccharide (LPS)-challenged mice models combined with 4D data-independent acquisition (DIA) proteomics to investigate the mechanisms by which SPD alleviates polarity loss in AEs. Our results demonstrated that SPD supplementation enhanced the antioxidant capacity and improved the villus/crypt ratio in the jejunum of LPS-treated mice. Proteomic analysis revealed that LPS induced acute phase and inflammatory responses, significantly downregulating the expression of cytoskeletal proteins (Pdlim3, Pdlim7) essential for epithelial morphology as well as proteins involved in apical–basal polarity (Pard6b, Pard3, Prkcz, LLGL2), apical membrane integrity (Vil1, Pdims, Akp3, Tjps, Pards), and apical SLC transporters. Conversely, SPD attenuated mucosal- and tissue-specific immune responses and reversed the downregulation of these protein groups. Furthermore, using a Caco-2 cell model, we confirmed the anti-inflammatory effect of SPD and elucidated its role in suppressing AE polarity loss via the regulation of HDAC4 signaling. These findings indicate that SPD effectively alleviates the inflammation-induced loss of AE polarity in the jejunum of LPS-challenged mice.

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