本文選題：谷氨酸　切入點(diǎn)：仔豬　出處：《武漢輕工大學(xué)》2015年碩士論文

【摘要】：本文研究了谷氨酸(Glu)對(duì)脂多糖(LPS)刺激仔豬腸道損傷及肌肉蛋白質(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G l u對(duì)LP S誘導(dǎo)的仔豬腸道損傷的保護(hù)作用,并從哺乳動(dòng)物雷帕霉素靶蛋白(m TOR)、Toll樣受體4(TLR4)和核苷酸結(jié)合寡聚域受體(NOD)信號(hào)通路的角度探討其作用機(jī)制。選擇24頭斷奶仔豬(杜?長(zhǎng)?大,平均體重7.02±0.21 kg),分為4個(gè)處理組:1)對(duì)照組;2)LP S+0%G l u組;3)LP S+1.0%G l u組;4)L P S+2.0%G l u組。試驗(yàn)期為28天。在正式試驗(yàn)第28天,2、3、4豬注射100μg/kg BW L P S,對(duì)照組注射等量的生理鹽水,4 h后屠宰,取腸道樣品待測(cè)。結(jié)果表明:Glu提高了空腸和回腸絨毛高度/隱窩深度、RNA/DNA、蛋白質(zhì)/DNA與及claudin-1蛋白表達(dá)量,也提高了回腸乳糖酶、麥芽糖酶和蔗糖酶活性,降低了空腸隱窩深度。Glu也降低了空腸TLR4、骨髓分化因子88(My D88)、白介素受體相關(guān)激酶1(IRAK1)、腫瘤壞死因子受體相關(guān)因子6(TRAF6)、NOD1、NOD2、受體互作蛋白激酶2(RIPK2)、核因子-κB(NF-κB)、Erbb2相互作用蛋白(ERBB2IP)、矢車菊苷β1(ACAP1)和回腸My D88、NOD1、細(xì)胞因子信號(hào)傳導(dǎo)抑制因子1(SOCS1)的m RNA表達(dá)量,提高了空腸Toll反應(yīng)蛋白(Tollip)和回腸白細(xì)胞分化抗原14(CD14)、Tollip的m RNA表達(dá)量。此外,G l u提高了空腸磷酸化m TO R(p-m T O R)/總m TO R(t-m TO R)和回腸p-m TO R/t-m T O R、總真核起始因子4 E結(jié)合蛋白1(t-4 E B P 1)蛋白表達(dá)量、磷酸化4EBP1(p-4EBP1)蛋白表達(dá)量。這些結(jié)果表明:Glu可通過激活m TOR信號(hào)通路,抑制TLR4和NOD信號(hào)通路,促進(jìn)蛋白質(zhì)合成,降低腸道炎性細(xì)胞因子的產(chǎn)生,從而緩解了LPS誘導(dǎo)的腸道損傷。2、本試驗(yàn)研究了G l u對(duì)LP S誘導(dǎo)的仔豬肌肉蛋白質(zhì)合成和降解的調(diào)控作用,并從TLR4和NOD、蛋白激酶B(Akt)/叉頭轉(zhuǎn)錄因子(FOXO)或m TOR信號(hào)通路的角度探討其機(jī)制。選擇24頭斷奶仔豬,分為4個(gè)處理組:1)對(duì)照組;2)LPS+0%Glu組;3)LPS+1.0%Glu組;4)L P S+2.0%G l u組。試驗(yàn)期為2 8天。在正式試驗(yàn)第2 8天,2、3、4組試驗(yàn)豬注射100μg/kg BW LPS,對(duì)照組注射等量的生理鹽水,4 h后屠宰,取肌肉樣品待測(cè)。結(jié)果表明:Glu提高了腓腸肌蛋白質(zhì)/DNA和背最長(zhǎng)肌蛋白質(zhì)含量、蛋白質(zhì)/DNA。Glu也降低了腓腸肌TLR4、IRAK1、R IP K 2、N F-κB和背最長(zhǎng)肌M y D 8 8、腫瘤壞死因子-α(T N F-α)的m R N A表達(dá)量。另外,Glu降低了背最長(zhǎng)肌FOXO1和FOXO4的m RNA表達(dá)量,使腓腸肌p-Akt/t-Akt和p-FOXO1/t-FOXO1上升。此外,Glu提高了腓腸肌p-m TOR/t-m TOR、p-4EBP1/t-4EBP1和背最長(zhǎng)肌p-4EBP1/t-4 E B P 1。這些結(jié)果表明:G l u可通過調(diào)控T L R 4和N O D信號(hào)通路,來調(diào)控炎性細(xì)胞因子的產(chǎn)生,或通過影響Akt/FOXO或m TOR信號(hào)通路,最終緩解肌肉蛋白質(zhì)的降解,促進(jìn)肌肉蛋白質(zhì)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 鹵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- 偽 T NF- 偽), 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.
【學(xué)位授予單位】：武漢輕工大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：S828.5

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