4.7 Article

Thiamine Supplementation Alleviates Lipopolysaccharide-Triggered Adaptive Inflammatory Response and Modulates Energy State via Suppression of NFκB/p38 MAPK/AMPK Signaling in Rumen Epithelial Cells of Goats

Journal

ANTIOXIDANTS
Volume 11, Issue 10, Pages -

Publisher

MDPI
DOI: 10.3390/antiox11102048

Keywords

thiamine; rumen epithelial cells; inflammation; energy metabolism; mitochondrial function

Funding

  1. National Natural Science Foundation of China [31872988, 31572429]
  2. Excellent Doctoral Dissertation Fund of Yangzhou University
  3. International Academic Exchange Fund for Graduate Students of Yangzhou University

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Studies have shown that exogenous thiamine supplementation can alleviate inflammation and promote rumen epithelial development in goats and cows. This study aimed to evaluate the effects of thiamine supplementation on LPS-induced inflammation and energy metabolic dysregulation in goat rumen epithelial cells. The results suggested that thiamine possesses anti-inflammatory and metabolic-modulatory effects, which are largely related to the suppression of the NF-kappa B/p38 MAPK/AMPK signaling pathway. Thiamine supplementation can also inhibit LPS-induced oxidative damage and apoptosis to protect mitochondrial function in rumen epithelial cells.
Studies have shown that exogenous thiamine (THI) supplementation can alleviate inflammation and promote rumen epithelial development in goats and cows. This research aimed to evaluate the effect of THI supplementation on LPS-induced inflammation and energy metabolic dysregulation in RECs of goats. Cells were stimulated with either 5 mu g/mL THI for 18 h (THI group) or with 5 mu g/mL LPS for 6 h (LPS group). The CON group was stimulated with DMEM/F-12 medium without THI for 18 h. The LPTH group was pretreated with THI for 18 h, followed by LPS stimulation for 6 h. THI supplementation decreased the ROS content (p < 0.05), as well as the ratios of phosphorylated (p)-p65 to p65 (p < 0.05) and p-AMPK alpha to AMPK alpha (p < 0.05). Interestingly, when the p38 gene was overexpressed in the LPTH group, the ratio of p-p65 to p65 and p-AMPK alpha to AMPK alpha proteins significantly increased, and ATP content decreased (p < 0.05). Our results suggest that THI possesses anti-inflammatory and metabolic-modulatory effects in RECs. The mechanism is largely related to the suppression of the NF-kappa B/p38 MAPK/AMPK signaling pathway. Additionally, we also revealed that THI supplementation can inhibit LPS-induced oxidative damage and apoptosis to protect mitochondrial function in RECs.

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