甘氨酸對脂多糖刺激的仔豬腸道損傷及肌肉蛋白質(zhì)合成和降解的調(diào)控作用
發(fā)布時(shí)間：2019-02-16 03:21
【摘要】：本文研究了甘氨酸(Gly)對脂多糖(LPS)刺激斷奶仔豬腸道損傷和肌肉蛋白質(zhì)合成和降解的調(diào)控作用及其機(jī)制。1、本試驗(yàn)研究了Gly對LPS刺激斷奶仔豬腸道損傷的影響,并從AMP激活蛋白激酶(AMPK)、哺乳動(dòng)物雷帕霉素靶蛋白(mTOR)、Toll樣受體(TLR4)和核苷酸結(jié)合寡聚域受體(NOD)信號通路的角度探討其作用機(jī)制。試驗(yàn)選用24頭斷奶仔豬,分為4個(gè)處理組:(1)對照組;(2)LPS組;(3)LPS+1.0%Gly組;(4)LPS+2.0%Gly組。試驗(yàn)第28 d,給2、3和4組注射100μg/kg BW的LPS,對照組注射等量的生理鹽水,4 h后屠宰,取腸道樣品待測。結(jié)果表明:1)Gly提高了空腸絨毛高度/隱窩深度比值,降低了空腸隱窩深度;2)Gly提高了空腸和回腸黏膜蛋白質(zhì)含量、蛋白質(zhì)/DNA比值和RNA/DNA比值;3)Gly提高了回腸檸檬酸合成酶和空腸異檸檬酸脫氫酶、α-酮戊二酸脫氫酶系活性;4)Gly降低了空腸和回腸AMPKα磷酸化水平,提高了回腸mTOR磷酸化水平;5)Gly降低了空腸TLR4、脂多糖結(jié)合蛋白(LBP)、髓樣分化因子88(MyD88)、腫瘤壞死因子(TNF)-α受體相關(guān)因子6(TRAF6)、NOD2、受體互作蛋白激酶2(RIPK2)、核因子(NF)-κB和回腸NOD2和RIPK2的mRNA表達(dá)量;6)Gly提高了空腸和回腸Toll樣反應(yīng)蛋白及回腸細(xì)胞因子信號傳導(dǎo)抑制因子1和Erbb2互作蛋白的mRNA表達(dá)量,降低了空腸矢車菊苷β1的mRNA表達(dá)量。以上結(jié)果表明,Gly可通過抑制TLR4和NOD信號通路降低了腸道炎癥反應(yīng),并通過調(diào)控AMPK和mTOR信號通路提高腸道蛋白質(zhì)的合成,緩解LPS刺激導(dǎo)致的腸道損傷。2、本試驗(yàn)研究了Gly對LPS刺激斷奶仔豬肌肉蛋白質(zhì)合成和降解的影響,并從AMPK、蛋白激酶B(Akt)/mTOR、Akt/叉頭轉(zhuǎn)錄因子(FOXO)及TLR4和NOD信號通路的角度探討其作用機(jī)制。試驗(yàn)選用24頭斷奶仔豬,分為4個(gè)處理組:(1)對照組;(2)LPS組;(3)LPS+1.0%Gly組;(4)LPS+2.0%Gly組。試驗(yàn)第28 d,2、3、4組注射100μg/kg BW的LPS,對照組注射等量的生理鹽水,4 h后屠宰,取肌肉樣品待測。結(jié)果表明:1)Gly提高了腓腸肌和背最長肌蛋白質(zhì)含量、蛋白質(zhì)/DNA比值和腓腸肌RNA/DNA比值;2)Gly提高了腓腸肌Akt磷酸化水平,降低了腓腸肌t-Akt蛋白表達(dá)量,提高了腓腸肌和背最長肌AMPKα磷酸化水平;3)Gly提高了腓腸肌mTOR和eIF4E結(jié)合蛋白1的磷酸化水平。Gly降低了腓腸肌FOXO1、肌萎縮F-box和肌肉環(huán)指蛋白1及背最長肌FOXO1和FOXO4的mRNA表達(dá)量,并降低了背最長肌t-FOXO1蛋白表達(dá)量,提高了背最長肌FOXO1蛋白磷酸化水平;4)Gly降低了腓腸肌TLR4、MyD88、白介素受體相關(guān)激酶1、TRAF6、NOD2、RIPK2、NF-κB和TNF-α及背最長肌MyD88、TRAF6、NOD2和TNF-α的mRNA表達(dá)量。以上結(jié)果表明,Gly可通過抑制TLR4和NOD信號通路緩解肌肉炎癥反應(yīng)的發(fā)生,并通過調(diào)控Akt/m TOR、Akt/FOXO信號通路提高肌肉蛋白質(zhì)的合成,抑制肌肉蛋白質(zhì)降解。Gly對LPS刺激導(dǎo)致的肌肉蛋白質(zhì)降解的調(diào)控作用與其對AMPK的調(diào)控?zé)o關(guān)。
[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, 偽 -ketoglutarate dehydrogenase system, 4) Gly decreased the level of AMPK 偽 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)-偽 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 偽 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- 偽, MyD88,TRAF6,NOD2 and TNF- 偽 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.
【學(xué)位授予單位】：武漢輕工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S828.5
本文編號：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, 偽 -ketoglutarate dehydrogenase system, 4) Gly decreased the level of AMPK 偽 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)-偽 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 偽 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- 偽, MyD88,TRAF6,NOD2 and TNF- 偽 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.
【學(xué)位授予單位】：武漢輕工大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：S828.5
【參考文獻(xiàn)】
相關(guān)期刊論文 前3條
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