L-精氨酸对脂多糖诱导的断奶仔猪肠道黏膜屏障损伤的缓解作用

Alleviatory Effects of L-Arg on Intestinal Mucosal Barrier Damage of Weanling Piglets Induced by Lipopolysaccharide Challenge

试验研究L-精氨酸(L-Arg)对脂多糖(LPS)诱导的断奶仔猪肠道黏膜屏障损伤的缓解作用。选择21日龄断奶的杜×长×大断奶仔猪18头,平均体重(7.52±0.92)kg,采用单因子试验设计,分为3个组:基础日粮(对照组)、基础日粮+LPS(LPS组)和基础日粮+LPS+0.5%Arg组(0.5%Arg组)(每组6个重复,每个重复1头猪)。试验期为18d。试验第18天,LPS组和0.5%Arg组腹腔注射100μg/kg BW LPS,对照组注射等量的生理盐水。注射LPS后4h前腔静脉采血,屠宰,刮取小肠黏膜。结果表明:1)与对照组相比,LPS刺激显著降低十二指肠黏膜中二胺氧化酶(DAO)活性(P<0.05),与LPS组相比,0.5%Arg显著增加了十二指肠和回肠黏膜中DAO活性(P<0.05);2)与对照组相比,LPS对血浆D-乳酸含量无显著影响(P>0.05),而与LPS组相比,0.5%Arg显著降低了血浆中D-乳酸的含量(P<0.05);3)与对照组相比,LPS刺激显著增加了十二指肠黏膜中内皮素-1(ET-1)的含量(P<0.05),而与LPS组相比,0.5%Arg显著缓解了十二指肠黏膜中ET-1含量的上升(P<0.05);4)与对照组相比,LPS刺激显著增加了回肠黏膜中丙二醛(MDA)和空肠黏膜中还原型谷胱甘肽(GSH)的含量以及空肠黏膜中GSH与氧化型谷胱甘肽(GSSG)的比值(GSH/GSSG)(P<0.05),而与LPS组相比,0.5%Arg显著缓解了LPS导致的回肠黏膜MDA和空肠黏膜GSH含量的上升(P<0.05)。这表明,L-Arg可通过降低肠黏膜中ET-1含量、降低机体的过氧化水平来缓解LPS导致的肠道黏膜屏障损伤。

An experiment was conducted to study the effects of L-Arg on intestinal mucosal barrier damage induced by lipopolysaccharide （LPS） challenge in weanling piglets. Using single factorial experiment design,eighteen 21-day-old Duroc×Landrace×Yorkshine crossed-bred piglets with （7.52±0.92） kg were randomly allotted to 3 groups （6 replicates per group and 1 piglet per replicate） including basal diet （control group）,basal diet＋LPS （LPS group） and basal diet＋LPS＋0.5% Arg （0.5% Arg group）. The experiment lasted for 18 d. On day 18 of the experiment,piglets in LPS and 0.5% Arg groups were injected intraperitoneally with 100 μg/kg BW LPS,whereas piglets in control group were injected with an equivalent amount of physiological saline. Blood samples were collected 4 h after LPS challenge. Subsequently,the piglets were slaughtered to collect intestinal mucosa for analysis. The results showed as follows： 1） compared with control group,LPS challenge significantly decreased diamino oxidase （DAO） activity of duodenum mucosa （P〈0.05）,and 0.5% Arg significantly increased DAO activity of duodenum and ileum mucosa compared with LPS group （P〈0.05）; 2） compared with control group,LPS challenge had no significant effect on plasma level of D-lactate （P〈0.05）,whereas 0.5% Arg significantly decreased plasma level of D-lactate compared with LPS group （P〈0.05）; 3） compared with control group,LPS significantly increased endothelin-1 （ET-1） content of duodenum mucosa,and 0.5% Arg significantly alleviated the LPS-induced increase of ET-1 content in duodenum mucosa compared with LPS group （P〈0.05）; 4） compared with control group,LPS challenge significantly increased the malondialdehyde （MDA） content of ileum mucosa,the GSH content of jejunum mucosa and GSH/GSSG of jejunum mucosa （P〈0.05）,and 0.5% Arg significantly alleviated the increases of MDA in ileum mucosa and GSH in jejunum mucosa compared with LPS group. These results indicated that Arg has beneficial effects on alleviating intestinal mucosal barrier damage induced by LPS challenge by the protective effects of Arg associated with inhibiting ET-1 production and decreasing intestinal oxidative level.