Frontiers in veterinary science · 2026
Protective effects of chlorogenic acid against LPS-induced intestinal oxidative injury in mice via activation of the PI3K/Akt-Nrf2/HO-1 signaling axis.
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He Ying, Wu Yuhan, Wei Yue, Wang Yuan, Feng Caiping
Аннотация
INTRODUCTION: Oxidative stress is a key pathological cause of intestinal epithelial injury and related intestinal diseases. Chlorogenic acid (CGA), a natural polyphenol, has notable antioxidant activity. This study explored the multi-target protective effects of CGA on intestinal epithelial cells and mouse intestinal tissue against oxidative injury, as well as its underlying molecular mechanisms.
METHODS: Network pharmacology was applied to screen core targets and enriched pathways of CGA against oxidative stress. H₂O₂-induced MODE-K cell oxidative damage model and LPS-induced mouse intestinal injury model were constructed. CCK-8, biochemical detection, qPCR, molecular docking, Western blotting and histopathological assay were performed to verify the protective effects and related signaling pathways.
RESULTS: Network pharmacology predicted PI3K/Akt and Nrf2/HO-1 pathways as crucial targets. In vitro, CGA elevated cell viability, reduced oxidative injury markers, upregulated antioxidant factors, and regulated apoptosis-related proteins. CGA blocked Keap1-Nrf2 binding, activated Nrf2/HO-1 and promoted Akt phosphorylation. In vivo, CGA alleviated LPS-induced intestinal pathological injury, while PI3K inhibitor LY294002 reversed its protective effects, confirming the critical role of PI3K/Akt-Nrf2/HO-1 axis.
CONCLUSION: CGA exerts multi-target antioxidant and intestinal protective effects by inhibiting Keap1-Nrf2 interaction and activating PI3K/Akt-Nrf2/HO-1 signaling axis, mitigating intestinal oxidative injury. Our findings provide a mechanistic basis for the application of CGA as a functional food ingredient or dietary intervention to alleviate intestinal oxidative stress in livestock.
METHODS: Network pharmacology was applied to screen core targets and enriched pathways of CGA against oxidative stress. H₂O₂-induced MODE-K cell oxidative damage model and LPS-induced mouse intestinal injury model were constructed. CCK-8, biochemical detection, qPCR, molecular docking, Western blotting and histopathological assay were performed to verify the protective effects and related signaling pathways.
RESULTS: Network pharmacology predicted PI3K/Akt and Nrf2/HO-1 pathways as crucial targets. In vitro, CGA elevated cell viability, reduced oxidative injury markers, upregulated antioxidant factors, and regulated apoptosis-related proteins. CGA blocked Keap1-Nrf2 binding, activated Nrf2/HO-1 and promoted Akt phosphorylation. In vivo, CGA alleviated LPS-induced intestinal pathological injury, while PI3K inhibitor LY294002 reversed its protective effects, confirming the critical role of PI3K/Akt-Nrf2/HO-1 axis.
CONCLUSION: CGA exerts multi-target antioxidant and intestinal protective effects by inhibiting Keap1-Nrf2 interaction and activating PI3K/Akt-Nrf2/HO-1 signaling axis, mitigating intestinal oxidative injury. Our findings provide a mechanistic basis for the application of CGA as a functional food ingredient or dietary intervention to alleviate intestinal oxidative stress in livestock.