Abstract

The study aimed to investigate the effect of erdosteine on middle ear effusion in rats through mediating the Toll-like receptor 4 (TLR4) signaling pathway. Rats were injected with endotoxin to prepare the model of acute secretory otitis media (SOM). Then, they were divided into an acute SOM model group (model group, n = 15) and erdosteine treatment group (18 mg/kg, gavage, treatment group, n = 15). Besides, a normal group (n = 15) was set up. Two weeks later, routine biochemical indicators such as aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were detected. The inflammatory effusion due to otitis media was scored. The content of myeloperoxidase (MPO), matrix metalloproteinase (MMP), and tumor necrosis factor-beta (TNF-β) in middle ear lavage fluid was detected via enzyme-linked immunosorbent assay (ELISA). Additionally, histomorphological changes were observed with the help of hematoxylin-eosin (HE) staining, and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting assays were carried out to measure the expression levels of TLR4 pathway genes and proteins as well as the messenger ribonucleic acid (mRNA) expression levels of key factors for otitis media (mucin 2 (MUC2) and MUC5A). In the model group, the levels of AST, ALP, and glutamic-pyruvic transaminase (GPT) were significantly increased (p < 0.05). Besides, the content of MPO, MMP, and TNF-β was overtly raised in the model group (p < 0.05), while it was notably lowered in the treatment group (p < 0.05). In the treatment group, the cilia were slightly swollen, and inflammatory cells were fewer. The mRNA levels of MUC2, MUC5A, and pathway genes TLR4 and c-Jun N-terminal kinase (JNK) were elevated in the model group. In addition, the protein assay results revealed that the protein levels of TLR4 and JNK were evidently increased in the model group. Erdosteine can treat the middle ear effusion in rats by repressing the activation of the TLR4 signaling pathway.

Highlights

  • Secretory otitis media (SOM), the most common antibiotic infection in children, is a pathological condition of the middle ear

  • The results of gene expression detection showed that the model group exhibited raised messenger ribonucleic acid (mRNA) levels of Mucin 2 (MUC2), MUC5A, Toll-like receptor 4 (TLR4), and Jun N-terminal kinase (JNK) (p < 0:05), while the treatment group had decreased such levels (p < 0:05) (Figure 3), implying that in the case of otitis media, the pathway genes may be activated during the pathogenesis, which indicates the further progression of the disease

  • The results revealed that the score was 1 point in the normal group, without inflammation and effusion; close to 4 points in the model group, with severe inflammation and effusion; and basically close to 1 point in the treatment group, with mild inflammation and effusion

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Summary

Introduction

Secretory otitis media (SOM), the most common antibiotic infection in children, is a pathological condition of the middle ear. In such a case, there is effusion in the complete tympanic membrane, accompanied by signs of acute inflammation. SOM is caused by changes in the ciliary system in the middle ear, often due to eustachian tube malfunction It is ubiquitous, especially in children with cleft palate, and often associated with the development of URTI and other diseases [1,2,3]. The diagnosis and management of SOM greatly affect the health of children, the cost of care, and the overall use of antimicrobials.

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