The effects of cold exposure on the ileum mechanical barrier in mice and its mechanisms.
10.12047/j.cjap.6235.2022.053
- Author:
Meng-Meng LIU
1
;
Yan ZHANG
1
;
Zi-Wei ZHANG
1
;
Jian-Bin YUAN
1
;
Jing-Ru GUO
1
Author Information
1. Heilongjiang Bayi Agricultural University, Daqing 163319, China.
- Publication Type:Journal Article
- Keywords:
NF-κB pathway;
cold exposure;
ileum;
tight junction
- MeSH:
Animals;
Cytokines/metabolism*;
Ileum/metabolism*;
Intestinal Mucosa;
Mice;
NF-kappa B/metabolism*;
Tight Junctions/metabolism*
- From:
Chinese Journal of Applied Physiology
2022;38(3):279-283
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To study the mechanisms of cold exposure mediated ileum mechanical barrier injury in mice. Methods: Twenty mice were randomly divided into the control and cold exposure groups. Both the control and cold exposure groups were placed in the climate room with (24±2)℃ and 40% humidity. The mice in the cold exposure group were moved to the climate room at (4±2)℃ every day for 3 hours for three consecutive weeks. Three weeks later, the ileum tissues of mice were collected. Changes in ileum tissue structure were observed by hematoxylin-eosin staining and Masson staining. The related protein expression levels of the tight junction, inflammatory cytokines, and the NF-κB pathway were detected by Western blot. Results: Compared with the control group, the circular muscle layer of the ileum in cold exposed mice became thin, a large number of inflammatory cells infiltrated, the length of villi became short, the depth of recess was increased, and tissue fibrosis appeared. The expression levels of ideal tight junction-associated proteins in cold exposed mice were decreased significantly (P＜0.05), while the protein expression levels of IL-1β, IL-6 and phosphorescent p65 were increased significantly (P＜0.05). Conclusion: Cold exposure can damage the tight junction of the mouse ileum, destroy the integrity of the mechanical barrier and activate the NF-κB signaling pathway to promote the occurrence of the inflammatory response.
