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Sodium Butyrate Supplementation Alleviates the Adaptive Response to Inflammation and Modulates Fatty Acid Metabolism in Lipopolysaccharide-Stimulated Bovine Hepatocytes
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2018-06-07 00:00:00 , DOI: 10.1021/acs.jafc.8b01439
Tianle Xu 1 , Nana Ma 1 , Yan Wang 1 , Xiaoli Shi 2 , Guangjun Chang 1 , Juan J. Loor 3 , Xiangzhen Shen 1
Affiliation  

This study aimed to evaluate whether sodium butyrate (SB) attenuates the hepatic response to LPS-induced inflammation in bovine hepatocytes. Hepatocytes isolated from cows at ∼160 days in milk (DIM) were exposed to 0.5 mmol/L SB for 18 h as pretreatment. Cells pretreated with SB were used for the SB group, and those subjected to 4 μg/mL lipopolysaccharide (LPS) challenge for 6 h were used for the lipopolysaccharide pretreated with SB (LSB) group. The LPS-challenged hepatocytes showed increases in TNF-α and IL-6 production in culture medium (37 ± 11, P < 0.05); these increases were attenuated by pretreatment with SB in the LSB group (267 ± 4, P < 0.05). Compared to that in LPS-treated cells, the phospho-p65 and phospho-IκBα protein expression and nuclear translocation were suppressed when SB was added. Genes (SREBP1c, SCD1, and DGAT1) and proteins (SREBP1c and SCD1) related to fatty acid metabolism were upregulated in LSB cells compared to those in LPS-treated cells (P < 0.05). The ratios of phospho-AMPKα to AMPKα (0.32 ± 0.03 vs 0.70 ± 0.07) and phospho-ACCα to ACCα were decreased (0.81 ± 0.06 vs 2.06 ± 0.16) (P < 0.05) in the LSB group. SB pretreatment reversed the histone H3 deacetylation that was increased by LPS stimulation in bovine hepatocytes (0.54 ± 0.02 vs 1.27 ± 0.11, P < 0.05). Our results suggest that SB pretreatment suppresses the hepatocyte changes that occur during the LPS-induced inflammatory response, which is accompanied by enhanced fatty acid synthesis, downregulated fatty acid oxidation, and histone H3 deacetylation, thus neutralizing the negative effects of infection.

中文翻译:

补充丁酸钠可减轻脂多糖刺激的牛肝细胞对炎症的适应性反应并调节脂肪酸代谢。

这项研究旨在评估丁酸钠(SB)是否减弱了牛LPS引起的牛肝细胞炎症反应的肝反应。在约160天的牛奶(DIM)中从母牛分离出的肝细胞进行0.5 h / L SB预处理18 h。用SB预处理的细胞用于SB组,用4μg/ mL脂多糖(LPS)刺激6 h的细胞用于SB(LSB)组预处理的脂多糖。LPS攻击的肝细胞在培养基中的TNF-α和IL-6产量增加(37±11,P <0.05)。在LSB组中,通过SB预处理可减轻这些增加(267±4,P<0.05)。与LPS处理的细胞相比,添加SB可以抑制磷酸化p65和磷酸化IκBα蛋白的表达和核易位。与经LPS处理的细胞相比,LSB细胞中与脂肪酸代谢相关的基因(SREBP1cSCD1DGAT1)和蛋白质(SREBP1c和SCD1)被上调(P <0.05)。在LSB组中,磷酸-AMPKα与AMPKα的比率(0.32±0.03对0.70±0.07)和磷酸-ACCα与ACCα的比率降低(0.81±0.06对2.06±0.16)(P <0.05)。SB预处理逆转了牛肝细胞中LPS刺激增加的组蛋白H3脱乙酰基作用(0.54±0.02与1.27±0.11,P<0.05)。我们的结果表明,SB预处理可抑制LPS诱导的炎症反应过程中发生的肝细胞变化,并伴有脂肪酸合成增强,脂肪酸氧化下调和组蛋白H3脱乙酰化,从而中和了感染的负面影响。
更新日期:2018-06-07
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