A high-concentrate diet induces an inflammatory response and oxidative stress and depresses milk fat synthesis in the mammary gland of dairy cows
A high-concentrate diet induces an inflammatory response and oxidative stress and depresses milk fat synthesis in the mammary gland of dairy cows
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DOI：
10.3168/jds.2021-21066
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发表时间：
2022-05-11
影响因子：
3.5
通讯作者：
Chang, G.
中科院分区：
文献类型：
--
作者：
Ma, N.;Abaker, J. A.;Chang, G.
高精料日粮饲喂虽然能暂时提高产奶量，但可引起亚急性瘤胃酸中毒（SARA）、乳脂抑制等一系列代谢性疾病。本试验旨在研究高精料饲粮对奶牛乳腺炎症反应、氧化应激和乳脂合成的影响。选取12头患有瘤胃瘘管的荷斯坦奶牛，随机分为2组，每组6头，分别饲喂低精日粮（LC）和高精日粮（HC）。在试验第20和21天，采集瘤胃液测定pH，采集乳样进行乳成分分析和脂多糖（LPS）浓度测定。第21天采集乳腺静脉血检测LPS浓度。实验21 d结束时，采集乳腺组织，采用实时荧光定量PCR和western blot分析乳腺组织中炎症反应-、氧化应激-、乳脂合成相关基因和蛋白的表达情况。HC组瘤胃液pH显著低于LC组，且HC组2个时间点pH均低于5.6，说明高精料饲粮诱导了SARA。HC组大鼠外周血脂多糖浓度较LC组明显升高。对于炎症反应，HC组乳腺中促炎因子（IL-6和IL-1 α）和先天免疫因子（舌抗菌肽和气管抗菌肽）显著升高，TLR4-NF-kappa B信号通路被激活。对于氧化应激，HC日粮喂养后，乳腺静脉血和乳腺组织中丙二醛含量升高，乳腺静脉血中谷胱甘肽含量降低，乳腺组织和乳腺静脉血中超氧化物歧化酶活性和总抗氧化能力降低，乳腺中抗氧化酶和抗氧化转录因子核因子红样2 （NFE2L2）表达降低。在乳脂代谢方面，HC饲粮降低了乳样中乳脂含量和乳腺中甘油三酯含量，抑制了新生合成酶（ACACA和FASN）、长链脂肪酸转化酶（ACSL1和SCD）、脂肪酸转运蛋白（CD36、FATP、FABP3和LPL）、甘油三酯合成酶（AGPAT6、DGAT1和LPIN1）、脂滴释放酶（PLIN1）的表达。转录因子固醇调节元件结合蛋白（SREBP1）和过氧化物酶体增殖物激活受体（PPARG）。综上所述，HC饲粮可通过提高奶牛外周静脉LPS浓度、刺激炎症反应和氧化应激、抑制乳腺乳脂合成等方式诱导奶牛SARA。
Although high-concentrate diet feeding can temporarily increase milk production, it can cause a series of metabolic diseases, such as subacute ruminal acidosis (SARA) and milk fat depression. The main purpose of this experiment was to study the effects of a high-concentrate diet on the inflammatory response, oxidative stress, and milk fat synthesis in the mammary gland of dairy cows. Twelve Holstein cows equipped with rumen fistulas were randomly divided into 2 groups, each with 6 cows, fed a low-concentrate diet (LC) and a high-concentrate diet (HC). On d 20 and 21 of the experiment, rumen fluid was collected to measure pH, and milk samples were collected for milk component analysis and lipopolysaccharide (LPS) concentration testing. On d 21, mammary vein blood was collected to detect the LPS concentration. At the end of the 21-d experimental period, mammary gland tissue was collected, and the expression of inflammatory response-, oxidative stress-, and milk fat synthesis-related genes and proteins in the mammary gland was analyzed by real-time quantitative PCR and western blot. The pH of rumen fluid in the HC group was significantly lower than that in the LC group, and the pH of 2 time points in the HC group was lower than 5.6, indicating that a high-concentrate diet induced SARA. The LPS concentration of the peripheral blood in HC group increased significantly compared with that in the LC group. For the inflammatory response, the proinflammatory cytokines (IL-6 and IL-1 alpha) and innate immune factors (lingual antimicrobial peptide and tracheal antimicrobial peptide) in the mammary gland of the HC group were significantly increased, and the TLR4-NF-kappa B signaling pathway was activated. For oxidative stress, after HC diet feeding, the content of malondialdehyde in mammary vein blood and mammary gland tissue increased, the content of glutathione in mammary vein blood decreased, the activity of superoxide dismutase and the total antioxidant capacity in mammary gland tissue and mammary vein blood decreased, and the expression of antioxidant enzymes and antioxidant transcription factor nuclear factor, erythroid 2 like 2 (NFE2L2) in mammary gland decreased. For milk fat metabolism, HC diet feeding reduced the milk fat content in milk samples and the triacylglycerol content in the mammary gland and inhibited the expression of de novo synthase (ACACA and FASN), long-chain fatty acid converting enzymes (ACSL1 and SCD), fatty acid transporters (CD36, FATP, FABP3, and LPL), triacylglycerol synthase (AGPAT6, DGAT1, and LPIN1), lipid droplet releasing enzyme (PLIN1), and transcription factors sterol regulatory element binding protein (SREBP1) and peroxisome proliferator activated receptor gamma (PPARG). In summary, a HC diet can induce SARA with increased concentration of LPS in the peripheral vein, stimulate inflammatory reactions and oxidative stress, and inhibit milk fat synthesis in the mammary gland of dairy cows.