甘氨酸对脂多糖刺激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：2019-02-16 03:21
【摘要】：本文研究了甘氨酸(Gly)对脂多糖(LPS)刺激断奶仔猪肠道损伤和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Gly对LPS刺激断奶仔猪肠道损伤的影响,并从AMP激活蛋白激酶(AMPK)、哺乳动物雷帕霉素靶蛋白(mTOR)、Toll样受体(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。试验选用24头断奶仔猪,分为4个处理组:(1)对照组;(2)LPS组;(3)LPS+1.0%Gly组;(4)LPS+2.0%Gly组。试验第28 d,给2、3和4组注射100μg/kg BW的LPS,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:1)Gly提高了空肠绒毛高度/隐窝深度比值,降低了空肠隐窝深度;2)Gly提高了空肠和回肠黏膜蛋白质含量、蛋白质/DNA比值和RNA/DNA比值;3)Gly提高了回肠柠檬酸合成酶和空肠异柠檬酸脱氢酶、α-酮戊二酸脱氢酶系活性;4)Gly降低了空肠和回肠AMPKα磷酸化水平,提高了回肠mTOR磷酸化水平;5)Gly降低了空肠TLR4、脂多糖结合蛋白(LBP)、髓样分化因子88(MyD88)、肿瘤坏死因子(TNF)-α受体相关因子6(TRAF6)、NOD2、受体互作蛋白激酶2(RIPK2)、核因子(NF)-κB和回肠NOD2和RIPK2的mRNA表达量;6)Gly提高了空肠和回肠Toll样反应蛋白及回肠细胞因子信号传导抑制因子1和Erbb2互作蛋白的mRNA表达量,降低了空肠矢车菊苷β1的mRNA表达量。以上结果表明,Gly可通过抑制TLR4和NOD信号通路降低了肠道炎症反应,并通过调控AMPK和mTOR信号通路提高肠道蛋白质的合成,缓解LPS刺激导致的肠道损伤。2、本试验研究了Gly对LPS刺激断奶仔猪肌肉蛋白质合成和降解的影响,并从AMPK、蛋白激酶B(Akt)/mTOR、Akt/叉头转录因子(FOXO)及TLR4和NOD信号通路的角度探讨其作用机制。试验选用24头断奶仔猪,分为4个处理组:(1)对照组;(2)LPS组;(3)LPS+1.0%Gly组;(4)LPS+2.0%Gly组。试验第28 d,2、3、4组注射100μg/kg BW的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:1)Gly提高了腓肠肌和背最长肌蛋白质含量、蛋白质/DNA比值和腓肠肌RNA/DNA比值;2)Gly提高了腓肠肌Akt磷酸化水平,降低了腓肠肌t-Akt蛋白表达量,提高了腓肠肌和背最长肌AMPKα磷酸化水平;3)Gly提高了腓肠肌mTOR和eIF4E结合蛋白1的磷酸化水平。Gly降低了腓肠肌FOXO1、肌萎缩F-box和肌肉环指蛋白1及背最长肌FOXO1和FOXO4的mRNA表达量,并降低了背最长肌t-FOXO1蛋白表达量,提高了背最长肌FOXO1蛋白磷酸化水平;4)Gly降低了腓肠肌TLR4、MyD88、白介素受体相关激酶1、TRAF6、NOD2、RIPK2、NF-κB和TNF-α及背最长肌MyD88、TRAF6、NOD2和TNF-α的mRNA表达量。以上结果表明,Gly可通过抑制TLR4和NOD信号通路缓解肌肉炎症反应的发生,并通过调控Akt/m TOR、Akt/FOXO信号通路提高肌肉蛋白质的合成,抑制肌肉蛋白质降解。Gly对LPS刺激导致的肌肉蛋白质降解的调控作用与其对AMPK的调控无关。
[Abstract]:The effects of glycine (Gly) on intestinal injury and muscle protein synthesis and degradation induced by lipopolysaccharide (LPS) in weaned piglets were studied. 1. The effects of Gly on intestinal injury induced by LPS in weaned piglets were studied. The mechanism of AMP activated protein kinase (AMP) -activated protein kinase (AMP) (AMPK), mammalian rapamycin target protein (mTOR), Toll like receptor (TLR4) and nucleotide binding oligodeoxyribonucleotide domain receptor (NOD) signal pathway was discussed. 24 weaned piglets were divided into four groups: (1) control group, (2) LPS group, (3) LPS 1.0%Gly group and (4) LPS 2.0%Gly group. On the 28th day of the experiment, the control group of 100 渭 g/kg BW LPS, was injected with the same amount of normal saline, then slaughtered 4 hours later, and the intestinal samples were taken for test. The results showed that: 1) Gly increased the ratio of villi height to crypt depth and decreased the depth of jejunum crypt, 2) Gly increased the protein content, protein / DNA ratio and RNA/DNA ratio of jejunum and ileum mucosa. 3) Gly increased the activity of ileum citrate synthase and jejunum isocitrate dehydrogenase, 伪 -ketoglutarate dehydrogenase system, 4) Gly decreased the level of AMPK 伪 phosphorylation in jejunum and ileum, and increased mTOR phosphorylation level in ileum. 5) Gly decreased TLR4, lipopolysaccharide binding protein (LBP), myeloid differentiation factor 88 (MyD88), tumor necrosis factor (TNF)-伪 receptor related factor 6 (TRAF6), NOD2, receptor interaction protein kinase 2 (RIPK2), and decreased the expression of MyD88 in jejunum. Nuclear factor (NF)-魏 B and mRNA expression of NOD2 and RIPK2 in ileum; 6) Gly increased the expression of mRNA in jejunum and ileum Toll like reactive protein, ileal cytokine signal transduction suppressor 1 and Erbb2 interaction protein, and decreased the mRNA expression of jejunum cytosine 尾 1. These results suggest that Gly can reduce the intestinal inflammatory response by inhibiting TLR4 and NOD signaling pathway, and increase the synthesis of intestinal protein by regulating AMPK and mTOR signaling pathway, and alleviate the intestinal injury induced by LPS stimulation. The effects of Gly on protein synthesis and degradation in weaned piglets stimulated by LPS were studied, and the mechanism of AMPK, protein kinase B (Akt) / mTOR,Akt/ fork head transcription factor (FOXO), TLR4 and NOD signaling pathway was discussed. 24 weaned piglets were divided into four groups: (1) control group, (2) LPS group, (3) LPS 1.0%Gly group and (4) LPS 2.0%Gly group. On the 28th day, the rats in the control group were injected with 100 渭 g/kg BW of LPS,. The control group was slaughtered 4 hours later, and the muscle samples were taken to be tested. The results showed that: 1) Gly increased the protein content, protein / DNA ratio and RNA/DNA ratio of gastrocnemius muscle and longissimus dorsi muscle; 2) Gly increased the level of Akt phosphorylation in gastrocnemius muscle, decreased the expression of t-Akt protein in gastrocnemius muscle, and increased the AMPK 伪 phosphorylation level in gastrocnemius and longissimus dorsi muscle. 3) Gly increased the phosphorylation level of mTOR and eIF4E binding protein 1 in gastrocnemius muscle, Gly decreased the expression of F-box and ring finger protein 1 in gastrocnemius FOXO1, muscle and FOXO1 and FOXO4 in longissimus dorsi muscle. The expression of t-FOXO1 protein in the longissimus dorsi muscle was decreased and the phosphorylation level of FOXO1 protein in the longissimus dorsi muscle was increased. 4) Gly decreased the mRNA expression of TLR4,MyD88, interleukin receptor-associated kinase 1 TRAF6, NOD2, RIPK2, NF- 魏 B, TNF- 伪, MyD88,TRAF6,NOD2 and TNF- 伪 in gastrocnemius muscle. These results suggest that Gly can attenuate the occurrence of muscle inflammation by inhibiting TLR4 and NOD signaling pathway, and increase the synthesis of muscle protein by regulating Akt/m TOR,Akt/FOXO signaling pathway. Inhibition of muscle protein degradation. The regulation of Gly on muscle protein degradation induced by LPS has nothing to do with the regulation of AMPK.
【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
本文编号：2423989
[Abstract]:The effects of glycine (Gly) on intestinal injury and muscle protein synthesis and degradation induced by lipopolysaccharide (LPS) in weaned piglets were studied. 1. The effects of Gly on intestinal injury induced by LPS in weaned piglets were studied. The mechanism of AMP activated protein kinase (AMP) -activated protein kinase (AMP) (AMPK), mammalian rapamycin target protein (mTOR), Toll like receptor (TLR4) and nucleotide binding oligodeoxyribonucleotide domain receptor (NOD) signal pathway was discussed. 24 weaned piglets were divided into four groups: (1) control group, (2) LPS group, (3) LPS 1.0%Gly group and (4) LPS 2.0%Gly group. On the 28th day of the experiment, the control group of 100 渭 g/kg BW LPS, was injected with the same amount of normal saline, then slaughtered 4 hours later, and the intestinal samples were taken for test. The results showed that: 1) Gly increased the ratio of villi height to crypt depth and decreased the depth of jejunum crypt, 2) Gly increased the protein content, protein / DNA ratio and RNA/DNA ratio of jejunum and ileum mucosa. 3) Gly increased the activity of ileum citrate synthase and jejunum isocitrate dehydrogenase, 伪 -ketoglutarate dehydrogenase system, 4) Gly decreased the level of AMPK 伪 phosphorylation in jejunum and ileum, and increased mTOR phosphorylation level in ileum. 5) Gly decreased TLR4, lipopolysaccharide binding protein (LBP), myeloid differentiation factor 88 (MyD88), tumor necrosis factor (TNF)-伪 receptor related factor 6 (TRAF6), NOD2, receptor interaction protein kinase 2 (RIPK2), and decreased the expression of MyD88 in jejunum. Nuclear factor (NF)-魏 B and mRNA expression of NOD2 and RIPK2 in ileum; 6) Gly increased the expression of mRNA in jejunum and ileum Toll like reactive protein, ileal cytokine signal transduction suppressor 1 and Erbb2 interaction protein, and decreased the mRNA expression of jejunum cytosine 尾 1. These results suggest that Gly can reduce the intestinal inflammatory response by inhibiting TLR4 and NOD signaling pathway, and increase the synthesis of intestinal protein by regulating AMPK and mTOR signaling pathway, and alleviate the intestinal injury induced by LPS stimulation. The effects of Gly on protein synthesis and degradation in weaned piglets stimulated by LPS were studied, and the mechanism of AMPK, protein kinase B (Akt) / mTOR,Akt/ fork head transcription factor (FOXO), TLR4 and NOD signaling pathway was discussed. 24 weaned piglets were divided into four groups: (1) control group, (2) LPS group, (3) LPS 1.0%Gly group and (4) LPS 2.0%Gly group. On the 28th day, the rats in the control group were injected with 100 渭 g/kg BW of LPS,. The control group was slaughtered 4 hours later, and the muscle samples were taken to be tested. The results showed that: 1) Gly increased the protein content, protein / DNA ratio and RNA/DNA ratio of gastrocnemius muscle and longissimus dorsi muscle; 2) Gly increased the level of Akt phosphorylation in gastrocnemius muscle, decreased the expression of t-Akt protein in gastrocnemius muscle, and increased the AMPK 伪 phosphorylation level in gastrocnemius and longissimus dorsi muscle. 3) Gly increased the phosphorylation level of mTOR and eIF4E binding protein 1 in gastrocnemius muscle, Gly decreased the expression of F-box and ring finger protein 1 in gastrocnemius FOXO1, muscle and FOXO1 and FOXO4 in longissimus dorsi muscle. The expression of t-FOXO1 protein in the longissimus dorsi muscle was decreased and the phosphorylation level of FOXO1 protein in the longissimus dorsi muscle was increased. 4) Gly decreased the mRNA expression of TLR4,MyD88, interleukin receptor-associated kinase 1 TRAF6, NOD2, RIPK2, NF- 魏 B, TNF- 伪, MyD88,TRAF6,NOD2 and TNF- 伪 in gastrocnemius muscle. These results suggest that Gly can attenuate the occurrence of muscle inflammation by inhibiting TLR4 and NOD signaling pathway, and increase the synthesis of muscle protein by regulating Akt/m TOR,Akt/FOXO signaling pathway. Inhibition of muscle protein degradation. The regulation of Gly on muscle protein degradation induced by LPS has nothing to do with the regulation of AMPK.
【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
【参考文献】
相关期刊论文 前3条
1 Reza Rezaei;Weiwei Wang;Zhenlong Wu;Zhaolai Dai;Junjun Wang;Guoyao Wu;;Biochemical and physiological bases for utilization of dietary amino acids by young Pigs[J];Journal of Animal Science and Biotechnology;2013年02期
2 刘玉兰,李德发,龚利敏,张文志,马丹;免疫应激对断奶仔猪免疫和神经内分泌激素的影响[J];中国畜牧杂志;2004年04期
3 柳国胜,康举龄,陆大祥,关洁宾,钟小兰,杨方,刘硕,帅春,聂川,罗先琼,黄云祖;甘氨酸对脂多糖和缺氧诱导鼠坏死性肠炎的影响[J];中国病理生理杂志;2002年04期
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