摘要The study was conducted to investigate the regulatory mechanism of glutamine(Gin)on intestinal inflammation in an Escherichia coli lipopolysaccharide(E.coli LPS)-induced in vivo and in vitro models.Piglets(n=8)weaned at 21 d of age were fed a basal diet(control and LPS groups)or 1％Gin diet(Gin+LPS group)ad libitum for 4 weeks.On d 22,24,26 and 28,piglets in the LPS and Gin+LPS groups were intraperitoneally injected with E.coli LPS.Intestinal porcine epithelial cells(IPEC-J2)(n=6)induced by LPS were used to assess related mechanisms and compound C was used to inhibit adenosine 5'-monophosphate-activated protein kinase(AMPK)activity.Our current results showed that compared with the LPS treatment,the Gln+LPS treatment had better growth performance and greater villus height(P＜0.05),and the Gln+LPS treatment reduced the rate of diarrhea by 6.4％(P＜0.05);the Gln+LPS treatment decreased serum tumor necrosis factor(TNF-α),interleukin-6(IL-6),K+,cortisol and insulin levels,whereas increased(P＜0.05)serum immunoglobulin M and epidermal growth factor levels;the Gln+LPS treatment increased(P＜0.05)the expression of aquaporins and AMPK pathway-associated targets in the jejunum and ileum of piglets,whereas decreased the expression of ion trans-porters(P＜0.05).The in vitro results showed that 4 mmol/L Gin administration could inhibit(P＜0.05)cell apoptosis and interleukin-1β(IL-1β),IL-6 and TNF-α secretion in LPS-induced IPEC-J2 cells,promote(P＜0.05)mitochondrial respiratory metabolism and increase(P＜0.05)the number of mitochondria and mitochondrial membrane potential.The activity of AMPK was elevated by 70％to 300％in Gln-treated IPEC-J2 cells under LPS challenge or normal conditions.Our results indicate that pre-administration of Gln to piglets suppresses intestinal inflammation by modulating the crosstalk between AMPK activation and mitochondrial function.