CAJ | 학술논문

为了探讨α-酮戊二酸(AKG)能否缓解LPS慢性应激导致的仔猪小肠黏膜损伤及其机理,本试验研究了AKG对LPS慢性应激仔猪的小肠黏膜形态、血浆D-木糖的含量、血浆和小肠黏膜二胺氧化酶(DAO)活性及小肠黏膜mTOR及磷酸化的mTOR表达量的影响.18头(24±1)日龄健康断奶仔猪随机分成3个处理组(空白对照组、应激对照组、AKG组),每个处理6个重复.各组基础日粮一致,空白对照组和应激对照组饲喂基础日粮+1%淀粉,AKG组饲喂基础日粮+1%AKG.试验期为16 d.应激对照组和AKG组仔猪分别于第10、12、14和16天腹膜注射80μg·kg~(-1)BW的LPS,空白对照组注射相应剂量的灭菌生理盐水.第16天注射LPS 2 h后,按0.1g·kg~(-1)BW的剂量给仔猪灌服D-木糖溶液,注射LPS 3 h后,前腔静脉采血.第17天屠宰取小肠组织样,刮取肠黏膜及制作组织切片.结果表明:(1)与空白对照组相比,应激对照组十二指肠、空肠和回肠黏膜绒毛高度/隐窝深度、空肠和回肠磷酸化mTOR/mTOR(P-mTOR/mTOR)显著降低(P<0.05),血浆DAO活性显著升高(P<0.05).(2)与应激对照组相比,AKG组十二指肠、空肠和回肠黏膜绒毛高度/隐窝深度、空肠黏膜DAO活性、血浆D-木糖及十二指肠、空肠和回肠黏膜P-mTOR/mTOR显著升高(P<0.05).结果显示,日粮中添加1%AKG可在一定程度上改善仔猪的小肠组织学形态和吸收功能,缓解LPS慢性应激导致的仔猪小肠黏膜损伤,这与mTOR信号通路有关.
위료탐토α-동무이산(AKG)능부완해LPS만성응격도치적자저소장점막손상급기궤리,본시험연구료AKG대LPS만성응격자저적소장점막형태、혈장D-목당적함량、혈장화소장점막이알양화매(DAO)활성급소장점막mTOR급린산화적mTOR표체량적영향.18두(24±1)일령건강단내자저수궤분성3개처리조(공백대조조、응격대조조、AKG조),매개처리6개중복.각조기출일량일치,공백대조조화응격대조조사위기출일량+1%정분,AKG조사위기출일량+1%AKG.시험기위16 d.응격대조조화AKG조자저분별우제10、12、14화16천복막주사80μg·kg~(-1)BW적LPS,공백대조조주사상응제량적멸균생리염수.제16천주사LPS 2 h후,안0.1g·kg~(-1)BW적제량급자저관복D-목당용액,주사LPS 3 h후,전강정맥채혈.제17천도재취소장조직양,괄취장점막급제작조직절편.결과표명:(1)여공백대조조상비,응격대조조십이지장、공장화회장점막융모고도/은와심도、공장화회장린산화mTOR/mTOR(P-mTOR/mTOR)현저강저(P<0.05),혈장DAO활성현저승고(P<0.05).(2)여응격대조조상비,AKG조십이지장、공장화회장점막융모고도/은와심도、공장점막DAO활성、혈장D-목당급십이지장、공장화회장점막P-mTOR/mTOR현저승고(P<0.05).결과현시,일량중첨가1%AKG가재일정정도상개선자저적소장조직학형태화흡수공능,완해LPS만성응격도치적자저소장점막손상,저여mTOR신호통로유관.
This study was conducted to investigate the effects of α-ketoglutarate (AKG) on small intestinal morphology, plasma D-xylose concentration, activities of diamine oxidase (DAO) in plasma and intestinal mucosa, and expression of mammalian target of rapamycin (mTOR) with phosphorylation (P-mTOR/mTOR) in the piglets under lipopolysaccharide (LPS) challenge. Eighteen healthy crossbred (Duroc×Landrace×Yorkshire) piglets were randomly assigned into 3 treatment groups (6 replicates per group)：control group, LPS group and AKG group. The control and LPS groups were fed the basal diet+1% starch, and the AKG group was fed the basal diet+1% AKG. On d 10, 12, 14 and 16, the piglets in the LPS and AKG groups were injected intraperitoneally with LPS at 80 μg·kg~(-1)BW，whereas piglets in the control group were injected intraperitoneally with the same dose of physiological saline. On d 16, D-xylose was orally administrated to all pigs at the dose of 0.1g·kg~(-1)BW 2h after LPS challenge, and blood samples were collected 3 h after LPS challenge. All the piglets were sacrificed on d 17 to examine small intestinal morphology and collect intestinal mucosa for analysis. The results showed that. (1) Compared to the control group, the ratio of villus height to crypt depth in duodenum, jejunum and ileum, P-mTOR/mTOR in jejunal and ileal mucosa of LPS group significantly decreased (P< 0.05), while the activities of DAO in plasma significantly increased (P<0.05). (2) Compared to the LPS group, the ratio of villus height to crypt depth in the duodenum and jejunum ileum, activities of DAO in the jejunal mucosa, D-xylose content in plasma and P-mTOR/mTOR in duodenal, jejunal and ileal mucosa of AKG group significantly increased (P<0.05). In conclusion, dietary supplementation with 1％ AKG could improve small intestinal morphology and absorption function to some extent and alleviate the intestinal mucosal damage caused by LPS challenge in piglets, which were associated with mTOR signaling pathway.