Chlorogenic acid protects against lipopolysaccharide-induced ileal injury in piglets
The intestine is recognized as the ‘motor’ of sepsis, so protecting it is a critical goal in the prevention and treatment of sepsis. The aim of this study was to investigate the protective effects of chlorogenic acid (CGA) against intestinal injury in a piglet sepsis model induced by lipopolysaccharide (LPS). The weaned piglets were fed with 1 g CGA/kg diet for 21 days before 100 μg LPS/kg body weight administration. After 4 h postinjection, ileal samples were collected. LPS induced ileal morphology atrophy, inhibited the mRNA expression of tight junction proteins, impaired mitochondrial energy metabolism, and disrupted key genes expression involved in mitochondrial quality control mechanisms (i.e., mitochondrial biogenesis, mitochondrial dynamics and mitophagy). CGA supplementation improved ileal morphology, enhanced claudin 3 mRNA abundance, increased ATP production, mediated complex I and III levels, upregulated peroxisome proliferators-activated receptor gamma coactivator 1 alpha, estrogen-related receptor alpha, BCL2 interacting protein 3 like and PTEN induced kinase 1 transcriptional expression in piglets exposed to LPS challenge. These observations reveal the significant protective potential of CGA against LPS-induced intestinal injury through the improvement of intestinal integrity and mitochondrial function, which provides a theoretical basis for application research of the natural product CGA in intestinal sepsis of piglets.
Authors
- Jinxiu Yao
- Jinrong Wang (ORCID: https://orcid.org/0000-0002-1450-1784)
- Yidan Wang
- Zehao Li (ORCID: https://orcid.org/0000-0003-0008-194X)
- Jin Huang
- Xinru Yuan
- Zhihua Song
- Le Kang
- Yong Zhang
- Kang Cheng
Institutions
- Henan University of Technology (CN)
Publication Details
- Journal
- Frontiers in Animal Science
- Published
- 2026-03-27
- DOI
- https://doi.org/10.3389/fanim.2026.1759983
- Primary Topic
- Barrier Structure and Function Studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00