Zinc oxide influences intestinal integrity, the expressions of genes associated with inflammation and TLR4-myeloid differentiation factor 88 signaling pathways in weanling pigs
Zinc oxide influences intestinal integrity, the expressions of genes associated with inflammation and TLR4-myeloid differentiation factor 88 signaling pathways in weanling pigs
复制标题
氧化锌影响断奶仔猪的肠道完整性、炎症相关基因的表达和 TLR4-骨髓分化因子 88 信号通路
DOI：
10.1177/1753425913499947
复制
发表时间：
2014-07-01
期刊：
影响因子：
3.2
通讯作者：
Ke, Ya Lu
中科院分区：
文献类型：
--
作者：
Hu, Cai Hong;Song, Ze He;Ke, Ya Lu
本研究探讨了补充氧化锌（ZnO）是否可以通过TLR和NOD样受体信号通路减轻断奶引起的肠道损伤。12头早期断奶仔猪被分配到两个日粮处理（对照与2200 mg Zn/kg的ZnO）1周。结果表明，添加氧化锌可提高日增重和采食量，降低断奶后腹泻评分，增加空肠黏膜绒毛高度和绒毛高度与隐窝深度比，降低血浆二胺氧化酶活性和内毒素浓度。结果表明，添加ZnO的仔猪肠道TLR 4及其下游信号分子MyD 88、IL-1受体相关激酶1和TNF-α受体相关因子6的mRNA表达水平降低，肠道促炎细胞因子和趋化因子的表达水平也降低。虽然添加ZnO对NF-κ B p65 mRNA丰度没有影响，但ZnO可下调NF-κB p65蛋白表达。然而，ZnO补充对肠道NOD 1和NOD 2的表达没有影响，它们的衔接分子受体相互作用丝氨酸/苏氨酸蛋白激酶2，以及caspase-3和热休克蛋白70的蛋白表达。结果表明，ZnO对肠道完整性的保护作用与其通过抑制TLR 4-MyD 88信号通路，降低炎症相关基因的表达密切相关。
This study explored whether zinc oxide (ZnO) supplementation could alleviate weanling-induced intestinal injury through TLR and NOD-like receptor signaling pathways. Twelve early-weanling piglets were allotted to two dietary treatments (control vs 2200 mg Zn/kg from ZnO) for 1 wk. The results showed that supplemental ZnO improved daily gain and feed intake, decreased post weaning scour scores, increased villus height and villus height:crypt depth ratio at the jejunal mucosa, and decreased diamine oxidase activity and endotoxin concentration in plasma. The intestinal mRNA levels of TLR4 and its downstream signals, including MyD88, IL-1 receptor-associated kinase 1 and TNF-α receptor-associated factor 6, were decreased, and the expressions of intestinal pro-inflammatory cytokines and chemokines were decreased simultaneously in the ZnO-supplemented piglets. Although NF-κB p65 mRNA abundance was not affected by ZnO supplementation, NF-κB p65 protein expression was down-regulated by ZnO. However, ZnO supplementation had no effect on intestinal expressions of NOD1 and NOD2, and their adaptor molecule receptor-interacting serine/threonine-protein kinase 2, as well as protein expressions of caspase-3 and heat shock protein 70. The results indicated that the protective effects of ZnO on intestinal integrity were closely related to decreasing the expressions of genes associated with inflammation through inhibiting the TLR4-MyD88 signaling pathways.