·To explore the expression characteristics of silent information regulator transcript 1 (SIRT1) in intestinal tissues of necrotizing enterocolitis (NEC), and preliminarily discuss the effect and possible mechanisms of SIRT1 in NEC.
·From June 2018 to October 2020, 80 children with NEC who were treated by neonatal surgery in the Children's Hospital, Zhejiang University School of Medicine were divided into observation group and control group. The tissue samples of the observation group were inflammatory necrotic intestinal tubes, while those of the control group were incised intestinal tubes. The NEC children in the control group were with intestinal strictures after conservative treatment, and then were treated by surgery again. The clinical data of the two groups were collected 24 h before surgery, including procalcitonin (PCT), hypersensitive C reactive protein (hs-CRP), cytokines [interleukin-2 (IL-2), IL-4, IL-6, IL-10, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)] in the serum, gender, gestational age and so on. The expression characteristics of SIRT1, nuclear factor-κB (NF-κB), transforming growth factor β1 (TGF-β1) and Smad3 proteins of the tissues in the two groups were detected by immunohistochemistry. IEC-6 cells of small intestinal epithelium of SD female rats were cultured in vitro. After SIRT1 expression in IEC-6 cells was inhibited by small interfering RNA (siRNA) technology, the protein expression of NF-κB was detected by Western blotting and the effects of SIRT1 on IEC-6 cells were detected by Cell Counting Kit-8 (CCK8) and Transwell migration assay.
·There was no significant difference in gender, gestational age, birth weight and delivery mode between the two groups. Compared with the control group, the levels of hs-CRP, PCT, IL-6 and IL-10 in the serum in the observation group increased within 24 h before surgery (all P=0.000).Compared with the margin tissues of narrow intestines in the control group, the positive expression of SIRT1 in NEC necrotic intestinal tissues in the observation group showed low expression, and the positive expression of NF-κB was overexpressed (both P=0.000). There was no significant difference in the expression of Smad3 and TGF-β1 between the two groups. The expression of SIRT1 in NEC necrotic intestinal tissue was negatively correlated with the expression of NF-κB (r=-0.592, P=0.000). After inhibiting the mRNA and protein expression of SIRT1, the relative expression of NF-κB in IEC-6 cells was increased, and the proliferation and migration ability of the cells was significantly decreased.
·The mechanism for the SIRT1 reducing progression of NEC may be that SIRT1 can inhibit the expression of NF-κB to reduce the expression of inflammatory factors in NEC, and another possible mechanism may be that SIRT1 can protect intestinal epithelial cells by promoting cell proliferation and migration.