脂多糖刺激对断奶仔猪肌肉炎症和蛋白质降解相关基因表达的影响

本试验旨在研究脂多糖(LPS)刺激后不同时间断奶仔猪肌肉炎症和肌肉蛋白质降解相关基因表达的变化规律。选择42头(7.1±0.9)kg杜×长×大三元杂断奶仔猪,按注射LPS之前(0 h)和注射LPS后1、2、4、8、12、24 h随机分为7个处理,每个处理6头猪。预试14 d后,腹腔注射100μg/kg体重的LPS。按以上时间点将仔猪屠宰,取背最长肌样品待测。结果表明:背最长肌炎性细胞因子肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-6的mRNA表达量在注射LPS 1～2 h后达到峰值;Toll样受体4信号通路关键基因Toll样受体4(TLR4)、骨髓分化因子88(MyD88),核苷酸结合寡聚域信号通路关键基因核苷酸结合寡聚域2(NOD2)、受体互作蛋白激酶2(RIPK2)的mRNA表达量在注射LPS 2～4 h后达到峰值;肌肉蛋白质降解相关基因叉头转录因子-1(FOXO-1)、FOXO-4、肌肉环指蛋白1(MuRF1)、肌萎缩F-box(MAFbx)的mRNA表达量在注射LPS 12 h后达到峰值。可见,LPS刺激诱导肌肉释放大量炎性细胞因子,使TLR4和NOD炎症信号通路关键基因及肌肉蛋白质降解相关基因mRNA显著表达。

Effects of Lipopolysaccharide Challenge on Genes Related to Muscle Inflammation and Protein Degradation of Weaned Piglets

The purpose of this study was to investigate the changes of genes related to muscle inflammation and protein degradation in weaned piglets at different time points after lipopolysaccharide(LPS) challenge. Forty-two weaned piglets(Duroc × Landrace × Yorkshine) with average body weight(7.1±0.9 kg) were randomly divided into seven groups. The piglets were injected with 100 μg/kg BW LPS, and slaughtered at 0 h(before LPS challenge), 1, 2, 4, 8, 12 and 24 h(after LPS challenge). The longissimus dorsi muscle samples were collected for analysis. The results showed that: the mRNA expression of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), IL-6 in longissimus dorsi muscle peaked at 1～2 h after LPS injection; The mRNA expression of the key genes in toll-like receptor 4(TLR4) and nucleotide binding oligomerization domin protein(NOD) signaling pathways including TLR4, myeloid differentiation factor 88(MyD88), receptor-interacting protein2(RIPK2) and NOD2 peaked at 2～4 h after LPS injection;(3) The mRNA expression of the key genes related to the muscle protein degradation including Forkhead Box O-1(FOXO-1), FOXO-4, muscle RING finger 1(MuRF1) and muscle atrophy F-box(MAFbx) peaked at 12 h after LPS injection. These results indicate that LPS induces the release of inflammatory cytokines in muscle, and increased mRNA expression of genes related to TLR4 and NOD inflammatory signaling pathways and muscle protein degradation.