LPS-induced reduction of triglyceride synthesis and secretion in dairy cow mammary epithelial cells via decreased SREBP1 expression and activity
LPS-induced reduction of triglyceride synthesis and secretion in dairy cow mammary epithelial cells via decreased SREBP1 expression and activity
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LPS 通过降低 SREBP1 表达和活性诱导奶牛乳腺上皮细胞甘油三酯合成和分泌减少
DOI：
10.1017/s0022029918000547
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发表时间：
2018
影响因子：
2.1
通讯作者：
Wu Rui
中科院分区：
文献类型：
--
作者：
Wang Jianfa;Zhang Xu;He Xianjing;Yang Bin;Wang Hai;Shan Xufei;Li Chunqiu;Sun Dongbo;Wu Rui
甾醇调节元件结合蛋白1（SREBP1）对乳脂合成具有核心调节作用。脂多糖（LPS）可诱发奶牛乳腺炎并导致乳脂率下降。已知SREBP1还与炎症调节有关。因此，在本研究中，我们假设LPS诱导的奶牛乳腺上皮细胞（DCMECs）乳脂率下降是通过降低SREBP1的表达和活性来实现的。为了验证这一假设，从奶牛乳腺组织中分离纯化DCMECs，并用LPS（10μg/ml）处理。LPS处理DCMECs抑制了脂质代谢相关转录因子SREBP1的mRNA表达、核转位和蛋白表达，导致甘油三酯含量降低。LPS处理后DCMECs中乙酰辅酶A羧化酶 - 1和脂肪酸合成酶的转录水平显著下调，表明参与从头合成乳脂的乙酰辅酶A羧化酶 - 1和脂肪酸合成酶受SREBP1调节。总之，这些结果表明LPS以时间依赖的方式通过降低SREBP1的表达诱导奶牛乳腺上皮细胞乳脂率下降。
Sterol regulatory element binding protein 1 (SREBP1) has a central regulatory effect on milk fat synthesis. Lipopolysaccharides (LPS) can induce mastitis and cause milk fat depression in cows. SREBP1 is also known to be associated with inflammatory regulation. Thus, in the current study, we hypothesized that LPS-induced milk fat depression in dairy cow mammary epithelial cells (DCMECs) operates via decreased SREBP1 expression and activity. To examine the hypothesis, DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS (10 mu g/ml). LPS treatment of DCMECs suppressed lipid-metabolism-related transcription factor SREBP1 mRNA expression, nuclear translocation and protein expression, leading to reduced triglyceride content. The transcription levels of acetyl-CoA carboxylase-1 and fatty acid synthetase were significantly down-regulated in DCMECs after LPS treatment, suggesting that acetyl-CoA carboxylase-1 and fatty acid synthetase involved in de novo milk fat synthesis was regulated by SREBP1. In summary, these results suggest that LPS induces milk fat depression in dairy cow mammary epithelial cells via decreased expression of SREBP1 in a time-dependent manner.