Cis-9, Trans-11 CLA Alleviates Lipopolysaccharide-Induced Depression of Fatty Acid Synthesis by Inhibiting Oxidative Stress and Autophagy in Bovine Mammary Epithelial Cells.
Cis-9, Trans-11 CLA Alleviates Lipopolysaccharide-Induced Depression of Fatty Acid Synthesis by Inhibiting Oxidative Stress and Autophagy in Bovine Mammary Epithelial Cells.
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Cis-9、Trans-11 CLA 通过抑制牛乳腺上皮细胞的氧化应激和自噬来减轻脂多糖诱导的脂肪酸合成抑制
DOI：
10.3390/antiox11010055
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发表时间：
2021-12-27
期刊：
影响因子：
--
通讯作者：
Shen X
中科院分区：
文献类型：
--
作者：
Ma N;Wei G;Zhang H;Dai H;Roy AC;Shi X;Chang G;Shen X
脂多糖（LPS）是革兰氏阴性菌的主要内毒素，可引起乳腺炎。牛乳腺上皮细胞（BMEC）是乳腺的主要组成部分，常受到LPS的攻击。顺式-9，反式-11共轭亚油酸（CLA）具有抗炎作用，但其在LPS刺激下维持BMEC细胞稳态的抗氧化能力有限。因此，我们研究了cis-9，trans-11 CLA是否可以恢复由LPS引起的氧化还原状态和自噬水平所指示的细胞内稳态的紊乱，并对细胞功能-乳脂代谢产生影响。对于氧化应激，LPS刺激促进活性氧（ROS）和硫代巴比妥酸反应物质（TBARS）的形成，并降低谷胱甘肽的浓度。LPS还在mRNA和蛋白水平上抑制了转录因子核因子2样红细胞2（Nrf 2）调节的抗氧化信号传导。而cis-9，trans-11 CLA预处理则下调了ROS和TBARS的形成，上调了抗氧化酶的表达。自噬作为天然免疫的一部分，也受到LPS刺激的激发，而CLA降低了自噬水平。LPS和H2 O2抑制乳脂合成相关转录因子固醇调节元件结合蛋白（SREBP 1）、过氧化物酶体增殖物激活受体γ（PPARG）及其下游酶。50 μ M cis-9，trans-11 CLA促进BMEC中乳脂合成相关基因的mRNA和蛋白质丰度以及脂滴形成。结论：LPS刺激可破坏BMEC细胞内环境稳定，抑制乳脂合成;而cis-9，trans-11 CLA可减轻氧化应激，降低自噬水平，促进乳脂合成，为乳腺炎的治疗提供了一种天然的策略。
Lipopolysaccharide (LPS) is the dominating endotoxin of Gram-negative bacteria, which can cause mastitis. Bovine mammary epithelial cells (BMECs), as major components of the mammary gland, usually suffer LPS challenge. Cis-9, trans-11 conjugated linoleic acid (CLA) has been reported to have anti-inflammatory characteristics, while its anti-oxidative ability to maintain cellular homeostasis in BMECs under LPS challenge is limited. Therefore, we studied whether cis-9, trans-11 CLA can restore the disturbance of cellular homeostasis indicated by the redox status and autophagy level caused by LPS and have an effect on cellular function- milk fat metabolism. For oxidative stress, LPS challenge promoted the formation of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) and decreased the concentration of glutathione. Anti-oxidative signaling regulated by transcription factor nuclear factor, erythroid 2 like 2 (Nrf2) was also depressed by LPS at the mRNA and protein level. However, cis-9, trans-11 CLA pretreatment downregulated the formation of ROS and TBARS and upregulated the expression of antioxidative enzymes. As a part of innate immunity, autophagy was also motivated by LPS challenge, while CLA decreased the autophagy level. LPS and H2O2 inhibited milk fat synthesis-related transcription factor sterol regulatory element binding protein (SREBP1), peroxisome proliferator activated receptor gamma (PPARG) and their downstream enzymes. Furthermore, 50 uM cis-9, trans-11 CLA promoted the mRNA and protein abundance of milk fat synthesis-related genes and lipid droplet formation in BMECs. In conclusion, LPS challenge disturbed the cellular homeostasis and depressed milk fat synthesis in BMECs; while cis-9, trans-11 CLA alleviated oxidative stress and decreased autophagy level, thus promoting milk fat synthesis, which offers a natural therapeutic strategy for mastitis.
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影响因子：
3.5
作者：
Basirico, L.;Morera, P.;Bernabuccri, U.
通讯作者：
Bernabuccri, U.
影响因子：
2.7
作者：
Gross, J. J.;Grossen-Roesti, L.;Bruckmaier, R. M.
通讯作者：
Bruckmaier, R. M.
DOI：
10.3923/pjbs.2013.1653.1661
发表时间：
2013-12-01
期刊：
Pakistan journal of biological sciences : PJBS
影响因子：
--
作者：
Deb, Rajib;Kumar, Amit;Kumar, Sushil
通讯作者：
Kumar, Sushil
影响因子：
5
作者：
Bergamo, Paolo;Palmieri, Gianna;Rossi, Mauro
通讯作者：
Rossi, Mauro
影响因子：
4.2
作者：
Chouinard, PY;Corneau, L;Bauman, DE
通讯作者：
Bauman, DE