Abstract Objective To study the effect of glutamine-supplemented enteral nutrition in regulating the apoptosis of intestinal mucosal cells and promoting mucosal healing in young rats with inflammatory bowl disease (IBD). Methods A total of 80 male Sprague-Dawley rats aged 4-5 weeks were randomly divided into 4 groups:blank control, IBD model, short peptide, and short peptide+glutamine (n=20 each). The IBD model was prepared by a single colon perfusion of 3-nitrobenzene sulfonic acid. At 3 days after modeling, the rats in the short peptide group were fed with short peptide formula (100 mL/kg), and those in the short peptide+glutamine group were fed with short peptide formula (100 mL/kg) and glutamine (0.5 g/kg). The course of intervention was 1 week. General conditions were observed after the experiment and their intestinal mucosal tissue was obtained. Hematoxylin-eosin staining was used to observe the pathological change of the intestinal mucosa. RT-PCR was used to measure the expression of apoptosis-regulating genes (bax and bc1-2) and apoptotic signal transduction factors (Caspase-3 and Caspase-9) in the intestinal mucosa. Western blot was used to measure the expression of insulin-like growth factor-1 (IGF-1) in the colonic mucosa. Results The IBD model group had poorer general conditions than the other three groups (blank control, short peptide and short peptide+glutamine), and the short peptide+glutamine group had better general conditions than the IBD model and short peptide groups. The IBD model group had significantly higher mRNA expression of bax than the other three groups (P < 0.05). There was no significant difference in the mRNA expression of bcl-2, Caspase-3 and Caspase-9 among the 4 groups (P > 0.05). The short peptide group had a significantly higher level of IGF-1 than the short peptide+glutamine, blank control and IBD model groups (P < 0.05). Conclusions Glutamine-supplemented enteral nutrition can effectively improve the general nutritional status of young rats with IBD, but it is not better than exclusive enteral nutrition in inhibiting the apoptosis of colonic mucosal cells and stimulating the synthesis of IGF-1 in the intestinal mucosa.
ZHAO Hong-Mei,OUYANG Hong-Juan,LIU Li et al. Effect of glutamine-supplemented enteral nutrition on the apoptosis of colonic mucosal cells in young rats with inflammatory bowl disease[J]. CJCP, 2019, 21(1): 89-93.
ZHAO Hong-Mei,OUYANG Hong-Juan,LIU Li et al. Effect of glutamine-supplemented enteral nutrition on the apoptosis of colonic mucosal cells in young rats with inflammatory bowl disease[J]. CJCP, 2019, 21(1): 89-93.
Sairenji T, Collins KL, Evans DV. An update on inflammatory bowel disease[J]. Prim Care, 2017, 44(4):673-692.
[3]
Fujita T, Sakurai K. Efficacy of glutamine-enriched enteralnutrition in an experimental model of mucosal ulcerativecolitis[J]. Br J Surg, 2005, 82(6):749-751.
[4]
Guan J, Harris P, Brimble M, et al. The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders[J]. Expert Opin Ther Targets, 2015, 19(6):785-793.
[5]
Morris GP, Beck PL, Herridge MS, et al. Hapten induced model of chronic inflammation and ulceration in the rat colon[J]. Gastroenterology, 1989, 96(3):795-811.
[6]
Oh SY, Cho KA, Kang JL, et al. Comparison of experimental mouse models of inflammatory bowel disease[J]. Int J Mol Med, 2014, 33(2):333-340.
[7]
Akobeng AK, Elawad M, Gordon M. Glutamine for induction of remission in Crohn's disease[J]. Cochrane Database Syst Rev, 2016, 8(2):CD007348.
[8]
Han T, Li XL, Cai DL, et al. Effects of glutamine-supplemented enteral or parenteral nutrition on apoptosis of intestinal mucosal cells in rats with severe acute pancreatitis[J]. Eur Rev Med Pharmacol Sci, 2013, 17(11):1529-1535.
Frater J, Lie D, Bartlett P, et al. Insulin-like growth factor 1(IGF-1) as a marker of cognitive decline in normal ageing:a review[J]. Ageing Res Rev, 2017, 9(42):14-27.
[11]
Xue H, Sufit AJ, Wischmeyer PE. Glutamine therapy improves outcome of in vitro andin vivo experimental colitis models[J]. Parenter Enteral Nutr, 2011, 35(2):188-197.
