miR-18a ameliorates inflammation and tissue injury in a mouse model of allergic rhinitis via blocking TLR4/NF-κB pathway.
- Author:
Jun YANG
1
;
Qingyun LI
1
;
Lu WANG
1
;
Hui XIE
2
Author Information
1. Clinical Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu 610036, China.
2. Clinical Medical College, Chengdu University of Traditional Chinese Medicine, Chengdu 610036, China. *Corresponding author, E-mail: Wangxie-ctu@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Mice;
Disease Models, Animal;
Inflammation;
Interleukin-6/genetics*;
MicroRNAs/genetics*;
NF-kappa B/metabolism*;
NF-KappaB Inhibitor alpha;
Rhinitis, Allergic;
RNA, Messenger;
Toll-Like Receptor 4/metabolism*;
Tumor Necrosis Factor-alpha/genetics*
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(8):680-685
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of microRNA-18a (miR-18a) in the pathogenesis of allergic rhinitis in mice. Methods Twenty-two BALB/c mice were randomly divided into a blank group, a model group and a miR-18a group. Mice in the model group and the miR-18a group were injected intraperitoneally with obumin (OVA) suspension to prepare allergic rhinitis models, and mice in the miR-18a group were simultaneously given lentiviral vector plasmid for overexpression of miR-18a. Allergy symptoms were evaluated by the behavioral score and HE staining. The plasma levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) were measured by ELISA. The distribution of CD45+ cells in nasal mucosa was measured by immunofluorescence histochemistry, and CD45+ cells in nasal lavage fluid were measured by flow cytometry. The mRNA expression levels of IL-1β, IL-6 and TNF-α in nasal mucosa tissues were measured by fluorescence quantitative PCR, and the protein expressions of Toll like receptor 4 (TLR4), nuclear factor κB p65 (NF-κB p65), inhibitor of NF-κB α (IκBα) and phosphorylated IκBα (p-IκBα) in nasal mucosa were measured by Western blot analysis. Results Compared with the blank group, the plasma levels of IL-1β, IL-6, and TNF-α in the model group increased significantly. The number of CD45+ cells in both nasal mucosa tissue and nasal irrigation fluid increased, and the mRNA levels of IL-1β, IL-6 and TNF-α and the protein expression levels of TLR4, NF-κB p65 and p-IκBα in nasal mucosa increased. Compared with the model group, the plasma levels of IL-1β, IL-6 and TNF-α in the miR-18a group decreased significantly. The number of CD45+ cells in both nasal mucosa tissue and nasal lavage fluid decreased, and the mRNA levels of IL-1β, IL-6 and TNF-α and the exprotein expression levels of TLR4, NF-κB p65 and p-IκBα in nasal mucosa decreased. Conclusion miR-18a can inhibit the occurrence and development of allergic rhinitis, and its molecular mechanism is related to the inhibition of TLR4/NF-κB pathway activation.
