Sodium Butyrate Alleviates Lipopolysaccharide-Induced Inflammatory Responses by Down-Regulation of NF-kappa B, NLRP3 Signaling Pathway, and Activating Histone Acetylation in Bovine Macrophages
FRONTIERS IN VETERINARY SCIENCE
Authors: Jiang, Liqiang; Wang, Jingjing; Liu, Ziyi; Jiang, Aimin; Li, Shuangqiu; Wu, Di; Zhang, Yong; Zhu, Xingyi; Zhou, Ershun; Wei, Zhengkai; Yang, Zhengtao
Abstract
Sodium butyrate is the sodium salt of butyric acid, which possesses many biological functions including immune system regulation, anti-oxidant and anti-inflammatory ability. The present study was designed to elucidate the anti-inflammatory effects and mechanisms of sodium butyrate on lipopolysaccharide (LPS)-stimulated bovine macrophages. The effect of sodium butyrate on the cell viability of bovine macrophages was assayed by using the CCK-8 kit. Quantitative real-time PCR (qRT-PCR) was used to detect the gene expression of interleukin-6 (IL-6), interleukin-1 beta (IL-1 beta), cyclooxygenase-2 (COX-2), and inducible Nitric Oxide Synthase (iNOS). NF-kappa B, NLRP3 signaling pathway, and histone deacetylase were detected by western blotting. The results showed that sodium butyrate had no significant effect on cell viability at 0-1 mM, and inhibited LPS-induced IL-6, IL-1 beta, COX-2, and iNOS expression. Moreover, sodium butyrate suppressed LPS (5 mu g/ml)-stimulated the phosphorylation of I kappa B and p65, inhibited the deacetylation of histone H3K9, and has also been found to inhibit protein expression in NLRP3 inflammasomes. Thus, our finding suggested that sodium butyrate relieved LPS-induced inflammatory responses in bovine macrophage by inhibiting the canonical NF-kappa B, NLRP3 signaling pathway, and histone decetylation, which might be helpful to prevent cow mastitis.
Long-lasting effects of postweaning sodium butyrate exposure on social behaviors in adult mice
BRAIN RESEARCH BULLETIN
Authors: Zhao, Penghui; Meng, Li; Dou, Mengxiao; Mao, Jiawen; Zhang, Ge; Zheng, Min; Yin, Xi; Tao, Zifei; Gong, Miao; Song, Li; Lian, Kaoqi; de-la-Paz, Omar Israel Velez; Guo, Qingjun; Shi, Haishui
Abstract
Background: The function of gut microbiota as its role in normal physiology and involvement in brain function has gained a great deal of attention. The potential long-lasting effects of postweaning sodium butyrate (SB) exposure on social behaviors are still unknown; however it acts as one of the metabolites of gut microbiota. Methods: Male mice (24-day old) were exposed to SB through drinking water for 21 continuous days. A series of behavioral tests, mainly including bedding preference test (BP), sexual preference test (SP), social interaction test (SI), tube dominance test (SDT), forced swimming test (FST), open field test (OFT), novel object recognition task (NOR) were conducted at different time after 21-d SB exposure. Serum Trimethylamine oxide (TMAO) levels were investigated to gain insight into a potential mechanism. Results: Behavioral results indicated that postweaning SB exposure significantly decreased the social dominance status of low-ranked mice and decreased the sexual preference without affecting social interaction. SB exposure also exerted transient anxiolytic-like effects, while having induced a long-lasting depression-like effect without effects on memory formation. Postweaning SB exposure increased serum TMAO levels in mice, especially in lower-ranked mice, but decreased in higher-ranked mice. Limitations: Lack of understanding of the underlying mechanism. Conclusions: These findings provide direct evidence, for the first time, that postweaning SB exposure produces long-term effects on social behaviors in adult mice, mainly referring to sexual orientation, social dominance, and depression-like behaviors, which may be related to the serum TMAO levels, highlighting the long-lasting po-tential effects of gut-brain interaction on social behaviors.