Zhou Wei, Li Wei, Zheng Xiao-Hui, Rong Xiao, Huang Long-Guang
Department of Neonatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Department of Pediatrics, Dongguan Taiping People's Hospital, Dongguan, China.
J Pediatr Surg. 2014 Jul;49(7):1057-63. doi: 10.1016/j.jpedsurg.2014.02.078. Epub 2014 Feb 26.
BACKGROUND/PURPOSE: Toll-like receptor (TLR)-4 and TLR-2 play an essential role in the pathogenesis of necrotizing enterocolitis (NEC). In this study, we investigated the protective effect of glutamine (Gln) in an NEC neonatal rat model, and the potential association with TLR-4 and TLR-2 expression in local intestinal tissues.
Preterm neonatal rats were randomly divided into 3 groups: normal control; NEC model; and NEC plus Gln intervention. NEC was induced by feeding with artificial milk substitutes, plus exposure to hypoxia and cold stress. All preterm rats were sacrificed at 3 days after birth. The intestinal tissues were taken for pathological analysis. Protein and mRNA expression of TLR-2, TLR-4, and caspase-3 was examined by immunohistochemistry and real-time RT-PCR, respectively.
Compared with the normal control, the NEC neonatal rats showed mucosal injury and upregulated mRNA and protein expression of TLR-2, TLR-4, and caspase-3 in ileum and colon. Gln intervention significantly reduced the mucosal injury and suppressed the upregulated expression of TLR-2, TLR-4, and caspace-3 in the ileum and colon of NEC neonatal rats.
Gln protects the intestinal tract of NEC neonatal rats, which may be associated with the reduction of TLR-2 and TLR-4 expression in intestines.
背景/目的:Toll样受体(TLR)-4和TLR-2在坏死性小肠结肠炎(NEC)的发病机制中起重要作用。在本研究中,我们调查了谷氨酰胺(Gln)在NEC新生大鼠模型中的保护作用,以及与局部肠道组织中TLR-4和TLR-2表达的潜在关联。
将早产新生大鼠随机分为3组:正常对照组;NEC模型组;NEC加Gln干预组。通过喂食人工代乳品,再加上缺氧和冷应激诱导NEC。所有早产大鼠在出生后3天处死。取肠道组织进行病理分析。分别通过免疫组织化学和实时逆转录聚合酶链反应检测TLR-2、TLR-4和半胱天冬酶-3的蛋白和mRNA表达。
与正常对照组相比,NEC新生大鼠表现出黏膜损伤,回肠和结肠中TLR-2、TLR-4和半胱天冬酶-3的mRNA和蛋白表达上调。Gln干预显著减轻了黏膜损伤,并抑制了NEC新生大鼠回肠和结肠中TLR-2、TLR-4和半胱天冬酶-3的上调表达。
Gln可保护NEC新生大鼠的肠道,这可能与肠道中TLR-2和TLR-4表达的降低有关。