1. miR-301a对小鼠坏死性小肠结肠炎的影响及作用机制.
- Author
-
邹大军, 胡福德, 周启立, and 徐晓青
- Abstract
Objective To investigate the effect and mechanism of miR-301a on necrotizing enterocolitis (NEC) in mice. Methods Sixty newborn BALB/c mice were randomly divided into the control group, the NEC group and the antagonist group (miR-301a antagonist group), with 20 mice in each group. NEC model was established in the NEC group and the miR-301a antagonist group by artificial feeding, hypoxia and cold stimulation for 5 days. The miR-301a antagonist group was given miR-301a antagonist on the basis of the NEC group. During the experiment, the body mass of mice was recorded, the histopathological changes of intestinal tissues were observed by HE staining in each group, and the inflammatory damage in intestinal tissues was scored. Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 were measured by enzyme-linked immunosorbent assay (ELISA) in each group. Apoptosis was measured by TUNEL method, and the protein expression levels of miR-301a and Caspase-1 were measured by qPCR and Western blot assay. Results Compared with the control group, mice in the NEC group showed reduced body mass, obvious inflammatory injury in intestinal tissue and increased intestinal tissue injury score. Serum levels of TNF- α, IL-6 and IL-8 were increased, apoptosis index of intestinal tissues were increased and mRNA and protein expression levels of miR-301a and Caspase-1 were also increased (all P < 0.05). Compared with the NEC group, mice in the miR-301a antagonistic group showed significantly reduced NEC symptoms, significantly decreased inflammatory injury score and serum levels of TNF- α, IL-6 and IL-8 in intestinal tissue, down-regulated apoptotic index of intestinal tissue and decreased expression levels of miR)301a and Caspase-1 (all P < 0.05). Conclusion miR-301a expression is increased in mouse NEC intestinal tissue, and downregulation of miR-301a could inhibit NEC progression in mice to a some extent. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF