Palmitic Acid and β-Hydroxybutyrate Induce Inflammatory Responses in Bovine Endometrial Cells by Activating Oxidative Stress-Mediated NF-κB Signaling
Palmitic Acid and β-Hydroxybutyrate Induce Inflammatory Responses in Bovine Endometrial Cells by Activating Oxidative Stress-Mediated NF-κB Signaling
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DOI：
10.3390/molecules24132421
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发表时间：
2019-07-01
期刊：
影响因子：
4.6
通讯作者：
He, Jianbin
中科院分区：
文献类型：
--
作者：
Li, Peng;Li, Lanzhi;He, Jianbin
酮症是奶牛的一种营养代谢疾病，研究表明酮症奶牛常伴有生殖问题。当酮症发生时，血液中的非酯化脂肪酸（NEFAs）和β -羟基丁酸（BHBA）水平显著增加。棕榈酸（PA）是构成NEFA的饱和脂肪酸的主要成分。本研究的目的是探讨高水平的PA和BHBA是否会诱导牛子宫内膜细胞（BEND）的炎症反应和调节机制。利用酶联免疫吸附试验、实时荧光定量PCR和western blotting，我们评估了不同浓度PA、BHBA、吡啶二硫代氨基甲酸酯（PDTC， NF-kappa B途径抑制剂）和n -乙酰半胱氨酸（NAC，抗氧化剂）处理的培养的BEND细胞的氧化应激、促炎因子和核因子(NF)-kappa B途径。处理细胞丙二醛含量显著升高，谷胱甘肽含量显著降低，抗氧化活性——谷胱甘肽过氧化物酶、超氧化物歧化酶、过氧化氢酶和总抗氧化能力均低于对照细胞。PA-和bhba诱导的氧化应激激活NF-kappa B信号通路，上调促炎因子的释放。此外，PA-和bhba诱导的nf - κ b介导的炎症反应被PDTC和NAC抑制。高浓度的PA和BHBA通过激活氧化应激介导的NF-kappa B信号传导诱导BEND细胞的炎症反应。
Ketosis is a nutritional metabolic disease in dairy cows, and researches indicated that ketonic cows always accompany reproductive problems. When ketosis occurs, the levels of non-esterified fatty acids (NEFAs) and beta-hydroxybutyrate (BHBA) in the blood increase significantly. Palmitic acid (PA) is a main component of saturated fatty acids composing NEFA. The aim of this study was to investigate whether high levels of PA and BHBA induce inflammatory responses and regulatory mechanisms in bovine endometrial cells (BEND). Using an enzyme-linked immunosorbent assay, quantitative real-time PCR, and western blotting, we evaluated oxidative stress, pro-inflammatory factors, and the nuclear factor (NF)-kappa B pathway in cultured BEND cells treated with different concentrations of PA, BHBA, pyrrolidinedithiocarbamate (PDTC, an NF-kappa B pathway inhibitor), and N-acetylcysteine (NAC, an antioxidant). The content of malondialdehyde was significantly higher, the content of glutathione was lower, and antioxidant activity-glutathione peroxidase, superoxide dismutase, catalase, and total antioxidant capacity-was lower in treated cells compared with control cells. PA- and BHBA-induced oxidative stress activated the NF-kappa B signaling pathway and upregulated the release of pro-inflammatory factors. Moreover, PA- and BHBA-induced activation of NF-kappa B-mediated inflammatory responses was inhibited by PDTC and NAC. High concentrations of PA and BHBA induce inflammatory responses in BEND cells by activating oxidative stress-mediated NF-kappa B signaling.