摘要
通过动物试验观察内毒素对肉鸡肠黏膜Na+-K+-ATPase活性影响及氨基胍的保护作用。30日龄黄羽肉鸡90只,随机分成内毒素处理组(LPS组,5mg/kg)、氨基胍治疗组(AG+LPS组)和生理盐水对照组。每组分别在处理后1、3、5、7和9h时间点杀鸡取样。取肠黏膜匀浆,提取线粒体。检测肠黏膜线粒体Na+-K+-ATPase活性。LPS在3、5h时,显著增加了肉鸡肠黏膜线粒体Na+-K+-ATPase活力(P<0.05),而在7、9h时,肠黏膜线粒体Na+-K+-ATPase活力却降至正常(P>0.05)。AG除了在5h时显著降低了肉鸡肠黏膜Na+-K+-ATPase活力外(P<0.05),其余时间点均显著增加了肉鸡肠黏膜线粒体Na+-K+-ATPase活力(P<0.05)。由此推论:LPS诱导了线粒体的损伤,引起线粒体内Na+-K+-ATPase活性紊乱,能量代谢障碍,组织机能发生改变;AG对LPS具有明显的拮抗作用,对机体起到保护作用。
To investigate the effect of LPS on activity of Na+-K+-ATPase in mitochondria of intes- tinal mucous membrane of broilers and the therapeutic action of aminoguanidine. A total of 90 30- day-old commercial broilers were divided randomly into three groups that were respectively treated with LPS (lipopolysaccharide from Salmonella typhimurium, 5 mg/kg), LPSq-AG (aminoguani- dine,300 mg/kg) and saline (2 mL/kg). After the injection of drugs,the mucous membrane of in- testine were taken from 6 killed birds per group at 1 h,3 h,5 h,7 h and 9 h. At every time point, the mitochondria as determined for the evaluations of the concentrations of Na+-K+-ATPase. The results indicated that LPS increased significantly the activity of Na+-K+-ATPase of the mitochon- dria in intestinal mucous membrane in broilers at 3 h and 5 h(P〈0. 05) ,but LPS didn't changed the activity at 7 h and 9 h(P〈0.05). After the injections of AG,the activity of Na+-K+-ATPase of the mitochondria in intestinal mucous membrane in broilers increased significantly at 1,3Tand 9 h(P〈0.05),but decreased at 5 h(P〈0.05). It might be concluded that the LPS induced the damnifieation of the mitochondria, resulting in the disfunetion of the energy metabolism, the de creased production of ATP energy, the impediment of the activity of Na+-K+-ATPase. AG playedan important role in the antigonism for the LPS.
出处
《中国兽医学报》
CAS
CSCD
北大核心
2013年第6期905-907,912,共4页
Chinese Journal of Veterinary Science
基金
中国博士后科学基金(2003033411)
河南省重点科技攻关(82102130014)
河南省高校杰出科研人才创新工程资助项目(2004KYCX019)