Chemico-biological interactions · 2026
Cinnamaldehyde alleviates LPS-induced endoplasmic reticulum stress-mediated barrier damage in IPEC-J2 by regulating calcium homeostasis.
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Wang Tian-Hao, Yang Zhou-Yi, Zhao Bi-Chen, Malhi Kanwar Kumar, Zhang Qing, Li Jian-Jie, Nie Feng-Qiu, Zhou Zhong-Fang, Shi Li-Jian, Wang Chun-Jiang, Li Jin-Long
Аннотация
BACKGROUND: Early weaning-induced intestinal barrier dysfunction is a major contributor to post-weaning diarrhea, growth retardation, and increased mortality in piglets, resulting in substantial economic losses and heavy reliance on antibiotic use in swine production. Cinnamaldehyde (Cin) is a plant essential oil that has been shown to promote intestinal health and may offer a potential alternative to antibiotics.
AIM: To investigate the probable mechanism underlying Cin's mitigating action on LPS-induced impairment of the integrity of the pig's small intestine epithelial barrier.
MATERIALS AND METHODS: IPEC-J2 cells were used as a model with four different treatment groups, and a 10 μM dose of Cin was selected to establish the model for alleviating intestinal barrier damage. After 24 h, barrier integrity, cell function, IP3R, ER stress markers, and intracellular Ca2+ were measured.
RESULTS: Cin alleviated LPS-induced cell cycle arrest, apoptosis, and proliferation inhibition. It restored barrier function, as evidenced by increased TEER, reduced FITC-Dextran 4 permeability, and upregulated expression of TJs. Mechanistically, Cin suppressed LPS-induced ER stress and ER expansion, downregulated IP3R expression, and reduced cytosolic Ca2+ overload. Correlation network analysis identified IP3R as a key link between ER stress and barrier dysfunction.
CONCLUSIONS: In summary, this study is the first to demonstrate that Cin exerts therapeutic effects on the injured IPEC-J2 barrier by regulating calcium homeostasis via IP3R. This study proposes new treatment strategies for restoring intestinal homeostasis disrupted by weaning stress in piglets.
AIM: To investigate the probable mechanism underlying Cin's mitigating action on LPS-induced impairment of the integrity of the pig's small intestine epithelial barrier.
MATERIALS AND METHODS: IPEC-J2 cells were used as a model with four different treatment groups, and a 10 μM dose of Cin was selected to establish the model for alleviating intestinal barrier damage. After 24 h, barrier integrity, cell function, IP3R, ER stress markers, and intracellular Ca2+ were measured.
RESULTS: Cin alleviated LPS-induced cell cycle arrest, apoptosis, and proliferation inhibition. It restored barrier function, as evidenced by increased TEER, reduced FITC-Dextran 4 permeability, and upregulated expression of TJs. Mechanistically, Cin suppressed LPS-induced ER stress and ER expansion, downregulated IP3R expression, and reduced cytosolic Ca2+ overload. Correlation network analysis identified IP3R as a key link between ER stress and barrier dysfunction.
CONCLUSIONS: In summary, this study is the first to demonstrate that Cin exerts therapeutic effects on the injured IPEC-J2 barrier by regulating calcium homeostasis via IP3R. This study proposes new treatment strategies for restoring intestinal homeostasis disrupted by weaning stress in piglets.