谷氨酸对脂多糖诱导的仔猪肠道损伤及肌肉蛋白质合成和降解的调控作用

发布时间：2018-03-31 08:30

本文选题：谷氨酸　切入点：仔猪　出处：《武汉轻工大学》2015年硕士论文

【摘要】：本文研究了谷氨酸(Glu)对脂多糖(LPS)刺激仔猪肠道损伤及肌肉蛋白质合成和降解的调控作用及其机制。1、本试验研究了G l u对LP S诱导的仔猪肠道损伤的保护作用,并从哺乳动物雷帕霉素靶蛋白(m TOR)、Toll样受体4(TLR4)和核苷酸结合寡聚域受体(NOD)信号通路的角度探讨其作用机制。选择24头断奶仔猪(杜?长?大,平均体重7.02±0.21 kg),分为4个处理组:1)对照组;2)LP S+0%G l u组;3)LP S+1.0%G l u组;4)L P S+2.0%G l u组。试验期为28天。在正式试验第28天,2、3、4猪注射100μg/kg BW L P S,对照组注射等量的生理盐水,4 h后屠宰,取肠道样品待测。结果表明:Glu提高了空肠和回肠绒毛高度/隐窝深度、RNA/DNA、蛋白质/DNA与及claudin-1蛋白表达量,也提高了回肠乳糖酶、麦芽糖酶和蔗糖酶活性,降低了空肠隐窝深度。Glu也降低了空肠TLR4、骨髓分化因子88(My D88)、白介素受体相关激酶1(IRAK1)、肿瘤坏死因子受体相关因子6(TRAF6)、NOD1、NOD2、受体互作蛋白激酶2(RIPK2)、核因子-κB(NF-κB)、Erbb2相互作用蛋白(ERBB2IP)、矢车菊苷β1(ACAP1)和回肠My D88、NOD1、细胞因子信号传导抑制因子1(SOCS1)的m RNA表达量,提高了空肠Toll反应蛋白(Tollip)和回肠白细胞分化抗原14(CD14)、Tollip的m RNA表达量。此外,G l u提高了空肠磷酸化m TO R(p-m T O R)/总m TO R(t-m TO R)和回肠p-m TO R/t-m T O R、总真核起始因子4 E结合蛋白1(t-4 E B P 1)蛋白表达量、磷酸化4EBP1(p-4EBP1)蛋白表达量。这些结果表明:Glu可通过激活m TOR信号通路,抑制TLR4和NOD信号通路,促进蛋白质合成,降低肠道炎性细胞因子的产生,从而缓解了LPS诱导的肠道损伤。2、本试验研究了G l u对LP S诱导的仔猪肌肉蛋白质合成和降解的调控作用,并从TLR4和NOD、蛋白激酶B(Akt)/叉头转录因子(FOXO)或m TOR信号通路的角度探讨其机制。选择24头断奶仔猪,分为4个处理组:1)对照组;2)LPS+0%Glu组;3)LPS+1.0%Glu组;4)L P S+2.0%G l u组。试验期为2 8天。在正式试验第2 8天,2、3、4组试验猪注射100μg/kg BW LPS,对照组注射等量的生理盐水,4 h后屠宰,取肌肉样品待测。结果表明:Glu提高了腓肠肌蛋白质/DNA和背最长肌蛋白质含量、蛋白质/DNA。Glu也降低了腓肠肌TLR4、IRAK1、R IP K 2、N F-κB和背最长肌M y D 8 8、肿瘤坏死因子-α(T N F-α)的m R N A表达量。另外,Glu降低了背最长肌FOXO1和FOXO4的m RNA表达量,使腓肠肌p-Akt/t-Akt和p-FOXO1/t-FOXO1上升。此外,Glu提高了腓肠肌p-m TOR/t-m TOR、p-4EBP1/t-4EBP1和背最长肌p-4EBP1/t-4 E B P 1。这些结果表明:G l u可通过调控T L R 4和N O D信号通路,来调控炎性细胞因子的产生,或通过影响Akt/FOXO或m TOR信号通路,最终缓解肌肉蛋白质的降解,促进肌肉蛋白质的合成。
[Abstract]:The regulation and mechanism of glutamate Glu-induced intestinal injury and muscle protein synthesis and degradation in piglets induced by lipopolysaccharide (LPS) were studied. The protective effect of GLU on LPs induced intestinal injury in piglets was studied. From the perspective of the signaling pathway of mammalian rapamycin target protein mTORO-Toll-like receptor (TLR4) and nucleotide binding oligodeoxyribonucleotide receptor (nod), 24 weaned piglets were selected. Long? Big, The average body weight was 7.02 卤0.21 kg / kg, divided into 4 treatment groups: control group (n = 1), control group (n = 2), control group (n = 2) and control group (n = 10) and control group (n = 4). The experimental period was 28 days. On the 28th day of the formal trial, 100 渭 g/kg BW LP was injected into 4 pigs, and the control group was injected with the same amount of raw material. After 4 hours of saltwater treatment, the butcher was slaughtered. The results showed that the activity of lactase, maltase and sucrase in ileum and jejunum increased with the increase of RNA / DNA, protein / protein expression and claudin-1 protein expression in jejunum and ileum villi, and the activity of lactase, maltase and sucrase in ileum. Decreased jejunal recess depth. Glu also decreased jejunum TLR4, bone marrow differentiation factor 88(My D88N, interleukin-receptor associated kinase 1- IRAK1, tumor necrosis factor receptor-associated factor 6TRAF6 nod _ 1 nod _ 2, receptor interacting protein kinase 2rIPK _ 2, nuclear factor- 魏 BNNF- 魏 -Erbb2 interaction protein, ERBB2IPV. The expression of m RNA was detected in 尾 1 尾 1 ACAP 1), my D88N NOD1, cytokine signal transduction suppressor 1 (SOCS1), and the expression of m RNA in the ileum. The expression of m RNA in jejunum Toll reactive protein Tollip and ileal leukocyte differentiation antigen 14 CD14 + Tollip was increased, and the phosphorylation of m to R(p-m T O O / total m to R(t-m o R in jejunum and p-m to R/t-m T O R in ileum and total eukaryotic initiation factor were increased. 4 E binding protein 1(t-4 E B P 1), These results suggest that TOR can activate m TOR signaling pathway, inhibit TLR4 and NOD signaling pathway, promote protein synthesis, and decrease the production of inflammatory cytokines in intestinal tract. In order to alleviate the intestinal injury induced by LPS, the regulation of GLU on protein synthesis and degradation in muscle of piglets induced by LP S was studied. The mechanism of TLR4 and nod, protein kinase B(Akt)/ forkhead transcription factor (FOXO) or m TOR signaling pathway was discussed. 24 weaned piglets were selected. The experimental period was 28 days. On the 28th day of the formal trial, 100 渭 g/kg BW LPSs were injected into the control group, and the control group was slaughtered with the same amount of normal saline for 4 hours. Muscle samples were taken to be tested. The results showed that the protein / DNA content of gastrocnemius muscle and the protein content of longissimus dorsi muscle were increased by 1: Glu. Protein / protein / DNA.Glu also decreased the mRNA expression of FOXO1 and FOXO4 in gastrocnemius muscle (TLR4IRAK1 / R IP K2F- 魏 B and M y D8 / 8, TNF- 伪 T NF- 伪), and decreased the expression of m RNA in the longissimus dorsi muscle (FOXO1 and FOXO4). P-Akt/t-Akt and p-FOXO1/t-FOXO1 were increased in gastrocnemius muscle. In addition, Glu increased the production of inflammatory cytokines in gastrocnemius muscle p-m TOR/t-m torus p-4EBP1 / t-4EBP1 and longissimus dorsi muscle p-4EBP1/t-4 E B P1. These results indicated that the production of inflammatory cytokines could be regulated by regulating the signal pathway of TLR _ 4 and N _ O _ D in gastrocnemius. Or by affecting the Akt/FOXO or m TOR signaling pathway, the degradation of muscle protein was alleviated and muscle protein synthesis was promoted.
【学位授予单位】：武汉轻工大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：S828.5

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