女贞子多糖对仔猪抗氧化及MAPK通路的影响

Studies on antioxidant and MAPK pathway of ligustrum polysaccharides in piglets

关键词:  女贞子多糖  仔猪  大肠杆菌病  抗氧化  MAPK通路

Key words:  Ligustrum polysaccharides  Piglets  Colibacillosis  Antioxidant  MAPK pathway

摘要:

为了研究女贞子多糖对人工感染大肠杆菌K88仔猪氧化应激的保护作用,将实验猪分为四组：对照组、模型组、女贞子多糖组和女贞子多糖饲喂后攻毒组。试验运用血清生化、ELISA和RT-PCR等技术,通过检测血清和肝肾组织的抗氧化酶和氧化产物,仔猪肝脏氧化应激相关基因转录水平和MAPK信号关键蛋白的转录,评价女贞子多糖的抗氧化机制。结果显示,女贞子多糖可以显著降低由大肠杆菌引起的仔猪血清MDA含量的升高,调节肝肾组织中MDA和SOD的水平；女贞子多糖可以提高仔猪肝脏中CAT和CuZnSOD转录水平；正常情况下,女贞子多糖对仔猪肝脏TNF-α的转录表达无影响,但可以降低大肠杆菌攻毒后的转录水平；激活MAPK通路主要依靠调控ERK1起作用。结论：女贞子多糖可以通过调节肝脏抗氧化指标保护大肠杆菌引起的仔猪氧化应激反应,其作用分子机制可能与下调MAPK相关信号转录水平有关。

Abstract:

In order to study the protective effect of ligustrum polysaccharide on oxidative stress of artificially infected piglets with E.coli K88, The experimental pigs were divided into four groups: control, model, ligustrum polysaccharide and ligustrum polysaccharide with E.coli.In this study, serum biochemical, ELISA and RT-PCR were used to detect antioxidant enzymes and oxidative products in serum and liver and kidney tissues, transcription level of genes related to liver oxidative stress in piglets, transcription of key proteins of MAPK signal, and antioxidant mechanism of ligustrumpolysaccharide.The results showed that theligustrum polysaccharide could significantly reduce the content of MDA in piglets caused by E.coli and regulate the level of MDA and SOD in liver and kidney tissues.The transcription of CAT and CuZnSOD in the livers of piglets can be improved by the polysaccharides of livers.Under normal circumstances, the expression of TNF-α in the liver of piglets was not affected by the polysaccharides of the livers, but the expression of the transcription of E.coli after challenge was reduced.Activation of MAPK pathway mainly depends on regulationof ERK1.Conclusion: ligustrum polysaccharide can protect piglet oxidative stress response induced by E.coli by regulating liver antioxidant index, and its molecular mechanism may be related to down-regulation of MAPK related signal transcription level.