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

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. C...

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Bibliographic Details
Main Authors: Yi Ma, Mawda Elmhadi, Chao Wang, Zelin Li, Hao Zhang, Banglin He, Xiujuan Zhao, Zhenbin Zhang, Hongrong Wang
Format: Article
Language:English
Published: MDPI AG 2022-10-01
Series:Antioxidants
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Online Access:https://www.mdpi.com/2076-3921/11/10/2048
Description
Summary: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 μg/mL THI for 18 h (THI group) or with 5 μg/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 (<i>p</i> < 0.05), as well as the ratios of phosphorylated (p)-p65 to p65 (<i>p</i> < 0.05) and p-AMPKα to AMPKα (<i>p</i> < 0.05). Interestingly, when the p38 gene was overexpressed in the LPTH group, the ratio of p-p65 to p65 and p-AMPKα to AMPKα proteins significantly increased, and ATP content decreased (<i>p</i> < 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-κB/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.
ISSN:2076-3921