Abstract

The study is aimed at observing the influence of microribonucleic acid- (miRNA-) 30a-50p on the pulmonary fibrosis in mice with Streptococcus pneumoniae infection through the regulation of autophagy by Beclin-1. Specific pathogen-free mice were instilled with Streptococcus pneumoniae through the trachea to establish the pulmonary fibrosis model. Then, they were divided into the miRNA-30a-50p mimics group (mimics group, n = 10) and miRNA-30a-5p inhibitors group (inhibitors group, n = 10), with the control group (n = 10) also set. Pulmonary tissue wet weight/dry weight (W/D) was detected. The content of tumor necrosis factor-α (TNF-α), interleukin- (IL-) 6, and myeloperoxidase (MPO) was determined using enzyme-linked immunosorbent assay (ELISA). Besides, the changes in the pulmonary function index dynamic lung compliance (Cdyn), plateau pressure (Pplat), and peak airway pressure (Ppeak) were monitored, and the gene and protein expression levels were measured via quantitative PCR (qPCR) and Western blotting. The expression level of miRNA-30a-5p was substantially raised in the mimics group (p < 0.05), but extremely low in the inhibitors group (p < 0.05). The mimics group had obviously raised levels of serum aminotransferase (AST), glutamic-pyruvic transaminase (GPT), alkaline phosphatase (ALP), and pulmonary tissue W/D (p < 0.05). Additionally, the expression levels of TNF-α, IL-6, and MPO were notably elevated in the mimics group, while their expression levels showed the opposite conditions in the inhibitors group (p < 0.05). According to the HE staining results, the inhibitors group had arranged orderly cells, while the mimics group exhibited lung injury, pulmonary edema, severe inflammatory response, and alveolar congestion. In the inhibitors group, Cdyn was remarkably elevated, but Pplat and Ppeak declined considerably (p < 0.05). Besides, the inhibitors group exhibited elevated messenger RNA (mRNA) levels of Beclin-1 and LC3, lowered mRNA levels of α-SMA and p62, a raised protein level of Beclin-1, and a markedly decreased protein level of p62 (p < 0.05). Silencing miRNA-30a-5p expression can promote the expression of Beclin-1 to accelerate the occurrence of autophagy, thereby treating pulmonary fibrosis in mice with Streptococcus pneumoniae infection.

Highlights

  • Idiopathic pulmonary fibrosis (IPF), a series of heterogeneous diffuse nonneoplastic diseases, initially occurs with the feature of alveolar epithelial cell injury and is accompanied by excessive migration, activation, and proliferation of fibroblasts in extracellular matrix remodeling [1, 2]

  • To observe the transfection efficiency of microribonucleic acid- (miRNA-)30a-5p in each group of mice, the gene expression level of microribonucleic acids (miRNAs)-30a-5p was measured in this study

  • According to the results (Figure 1), the expression level of miRNA-30a-5p was notably raised in the mimics group (p < 0:05), while it was Target gene glyceraldehyde-3-phosphate dehydrogenase (GAPDH) α-Smooth muscle actin (α-SMA) Beclin-1 LC3 p62 miRNA-30a-5p

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Summary

Introduction

Idiopathic pulmonary fibrosis (IPF), a series of heterogeneous diffuse nonneoplastic diseases, initially occurs with the feature of alveolar epithelial cell injury and is accompanied by excessive migration, activation, and proliferation of fibroblasts in extracellular matrix remodeling [1, 2]. IPF is generally considered to be a persistent damage-induced disease that is most likely to cause inflammation, and the expansion and proliferation of fibroblasts and deposition of extracellular matrix as well as irreversible obstructive pulmonary function decline, resulting in irreversible restrictive lung function deterioration and death [4]. It is a major breakthrough on this disease that macrolide treatment has been found to be able to prevent the progression of disease and even improve pulmonary function [5], which is, only applicable to the BioMed Research International patients with increased neutrophilic granulocytes in the airway. According to a study, blocking inflammation can prevent neutrophilic granulocytes from flowing into the airway, repressing pulmonary fibrosis [8]

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