Cell model for researching necrotizing enterocolitis and construction method of cell model

Abstract

The invention discloses a construction method of a cell model for research on necrotizing enterocolitis. The cell model is obtained by using virus to induce MYD88 gene silencing of cells. The method is simple, efficient, easy to operate and suitable for industrial popularization and application. The cell model for studying the necrotizing enterocolitis, which is constructed by the invention, can be stably used for studying the pathological mechanism of the necrotizing enterocolitis, has the advantages of simplicity, convenience, easiness in obtaining and low cost compared with an animal model, and provides a new choice for studying the necrotizing enterocolitis.

Description

technical field [0001] The invention specifically relates to a cell model and a construction method thereof for the study of necrotizing enterocolitis. Background technique [0002] Necrotizing enterocolitis is an acquired disease, mainly in premature or sick newborns, characterized by necrosis of the mucosa and even the deep layers of the bowel, most often in the terminal ileum and rarely in the colon and proximal small bowel Affected. In neonates who develop necrotizing enterocolitis, three factors are typically present in the small intestine: persistent intestinal ischemic damage, bacterial colonization, and luminal substrate (eg, enteral feeding). [0003] The cause of necrotizing enterocolitis is unknown. It is believed that intestinal ischemic damage disrupts mucus production in the gut, rendering the gut susceptible to bacterial attack, and once feeding begins, provides an ample substrate for gut bacteria to multiply, which can permeate the gut wall, produce hydroge...

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Problems solved by technology

[0004] The inventor's research on animal models obtained by knocking out the MYD88 gene confirmed that MYD88 can reduce the apoptosis of intestinal epithelial cells and reduce the occurrence of inflammation during the development of necrotizing enterocolitis, and published it in the "Chinese Journal of Pediatric Surgery" "Research on the Mechanism of the Key Protein MyD88 in the TLR4 Pathway in the Pathogenesis of Necrotizing Enterocolitis", but the occurrence and development of the disease is often the result of the joint action of multiple targets and links. Since the animal model is a complex individual, it affects its There are many factors in the disease process, which is not conducive to the accurate and objective analysis of each factor in the disease. Therefore, it is more important to construct a cell model with fewer influencing factors for the pathological mechanism of necrotizing enterocolitis and to screen therapeutic and / or preventive drugs. Due to the complexity of mutations at the molecular level, there is currently no cell model for stable MYD88 silencing

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