Regulatory Effect Of Aspartic Acid On Intestinal Injury In Piglets After Lipopolysaccharide Challenge

Two exp eriment s were condu cted to investigate the effects ofaspartic acid (ASP) supplementation o n intestinal structure and funct ionof weanling piglets after lipopol ys accharide (LPS) chall enge and itsmechanisms.1. Experiment1was conducted to ex plore the mechanis m (s) b ywhich ASP ex erted its protective role on intestinal dam age from theperspectiv e of en erg y m etabolism. Twen t y four pigs average bod y weight7.37±0.04kg were allotted to four treat ments including:(1) control group;(2) LPS group;(3) LPS+0.5%ASP gro u p;(4) LP S+1.0%AS P g ro u p. T h epigs were slaughtered after24h LP S challenge to co ll ect intestinalsamples for anal ysis. The results showed that:1)0.5%or1.0%A SPalleviated the decrease of jejunal villus height and villus height/cr yptdepth and the increase of cr ypt depth in duced b y LPS, and i ncreas ed ilealvillus height and vil lus height/cr ypt dep th (P<0.05).2)0.5%or1.0%A SPalleviated the decrease of jejunal protein/DNA and RNA/DNA and ilealprotein/DNA induced b y LPS (P <0.05).3)0.5%or1.0%A SP alleviatedthe decrease of jejunal sucrose activit y and ileal maltase act ivit y inducedb y LPS, and increased jejunal lactas e activit y and ileal lactas e andsucrose activities (P<0.05).4)0.5%A SP alleviated the decreas e of ADPand ATP contents an d the increas e of AMP/ATP in ileum induced b y LPS,and increased en erg y ch arg e, total ad en ine nucleotide, ATP and ADPcontents and redu ced AMP/ATP in j ejunum (P<0.05).5)0.5%ASPalleviated the decrease of jejunal and il eal isocitrate deh yd rogenase andα-ketoglutarate dehydrogenase complex activities induced by LPS, andincreas ed jejunal and ileal citrate s ynthase activit y (P <0.05).6)0.5%or1.0%ASP alleviated the increase o f th e mRNA expression of AMPKα1,AMPKα2, PGC1α and pAMPK/tAMPK ratio in ileum induced b y LPS, and reduced mRNA exp ression of AMPKα1, Sirt1and PGC1α in jejunum(P<0.05). Th ese res ults indicate that ASP can protect i ntes tinal structureand funct ion thro ugh improving intestinal energ y metabolism viamodulation of AMPK signal ing pathwa y.2. Experiment2was conducted to ex plore the mechanis m (s) b ywhich ASP ex erted its protective role on intestinal dam age from theperspective o f inflammatory response. Twent y four pigs average bod yweight8.07±0.75kg were allotted to four treatments including:(1)control group;(2) LPS group;(3) LPS+0.5%ASP group;(4) LPS+1.0%ASP group. The pigs were slaughtered after4h LPS challenge to collectintestinal samples for anal ysis. The results showed that:1)0.5%and1.0%ASP allevi ated the d ecrease of jejunal and ileal villus height/cr yptdepth and th e increase of ileal cr ypt d epth induced b y LPS (P<0.05).2)0.5%or1.0%A SP alleviated the d ecrease of ileal DAO activit y andjejunal protein expression of o ccludin and claudin-1indu ced b y LPS, andincreas ed jejunal DAO activit y (P<0.05).3)0.5%and1.0%ASPalleviated the increase of ileal caspase3protein expression (P<0.05).4)0.5%or1.0%ASP alleviated the increas e of jejunal mRNA expression ofM yD88, NOD2, R IPK2and NF-κB p65induced b y LPS, and reducedmRNA expression o f T LR4、 IR AK1an d TRAF6(P<0.05),0.5%or1.0%ASP also alleviated the increase of ileal mRNA expression of TRAF6andNOD2induced b y LPS, and redu ced mR NA expression of T LR4, M yD88and NOD1(P<0.05). These results indicate that ASP can prot ect i ntestinalstructure and funct ion through redu cing inflammator y response vi amodulation of T LRs and NODs signal in g pathway.