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MiR-31 aggravates inflammation and apoptosis in COPD rats via activating the NF-κB signaling pathway
1Department of Respiratory Medicine, Shaanxi Provincial People's Hospital, Xian, China. shanxiliwu@126.com.
Objective:
To study the effect of micro ribonucleic acid (miR)-31 on rats with chronic obstructive pulmonary disease (COPD) by activating the nuclear factor-κB (NF-κB) signaling pathway.
Materials And Methods:
A total of 36 Sprague-Dawley rats were randomly divided into normal group (n=12), model group (n=12) and miR-31 mimics group (n=12). The rats were fed normally in normal group. In model group, the COPD model was first established, followed by intervention using normal saline. In miR-31 mimics group, the COPD model was also first established, followed by intervention using miR-31 mimics. The expression of NF-κB was detected via immunohistochemistry. Protein expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were determined through Western blotting. Serum levels of interleukin-6 (IL-6), IL-18 and tumor necrosis factor-α (TNF-α) were measured via enzyme-linked immunosorbent assay (ELISA). Moreover, the apoptosis was examined via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and the relative expression of miR-31 was detected by means of quantitative polymerase chain reaction (qPCR).
Results:
The immunohistochemistry results showed that the positive expression of NF-κB was significantly higher in the other two groups than that in normal group (p<0.05), while it was also remarkably higher in miR-31 mimics group than that in model group (p<0.05). The results of Western blotting revealed that the relative protein expression of Bax significantly increased, while that of Bcl-2 notably declined in the other two groups compared with those in normal group (p<0.05). Similarly, the relative protein expression of Bax was upregulated, while that of Bcl-2 was distinctly reduced in miR-31 mimics group compared with those in model group (p<0.05). It was found via ELISA that the model group and miR-31 mimics group had evidently higher levels of IL-6, IL-18 and TNF-α than those in normal group (p<0.05), while miR-31 mimics group also had prominently higher levels than those in model group (p<0.05). In addition, according to the TUNEL assay, the apoptosis rate remarkably increased in the other two groups in comparison with that in normal group (p<0.05), while it remarkably rose in miR-31 mimics group compared with that in model group (p<0.05). Finally, a significantly higher expression of miR-31 was observed in the other two groups than that in normal group via qPCR (p<0.05), and such a higher expression was also found in miR-31 mimics group than that in model group (p<0.05).
Conclusions:
MiR-31 aggravates inflammation and apoptosis in COPD rats by activating the NF-κB signaling pathway.
Insights
Micro ribonucleic acid (miR)-31 exacerbates chronic obstructive pulmonary disease (COPD) in rats by activating the nuclear factor-κB (NF-κB) pathway, increasing inflammation and cell death.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Inflammation Research
Background:
- Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and airflow limitation.
- MicroRNAs (miRNAs) play crucial roles in regulating gene expression and are implicated in the pathogenesis of various diseases, including COPD.
- The nuclear factor-kappa B (NF-κB) signaling pathway is a key regulator of inflammation and cell survival, often dysregulated in COPD.
Purpose of the Study:
- To investigate the role of micro ribonucleic acid (miR)-31 in the development of chronic obstructive pulmonary disease (COPD) in a rat model.
- To determine whether miR-31 exerts its effects by activating the nuclear factor-κB (NF-κB) signaling pathway.
- To evaluate the impact of miR-31 on inflammation, apoptosis, and key protein expression in COPD rats.
Main Methods:
- Establishment of a COPD rat model and intervention with miR-31 mimics or saline.
- Assessment of NF-κB expression using immunohistochemistry.
- Quantification of Bcl-2 and Bax protein levels via Western blotting.
- Measurement of serum inflammatory cytokines (IL-6, IL-18, TNF-α) using ELISA.
- Evaluation of apoptosis through TUNEL assay and miR-31 expression via qPCR.
Main Results:
- miR-31 mimics significantly increased NF-κB expression, pro-apoptotic Bax, and inflammatory cytokines (IL-6, IL-18, TNF-α) in COPD rats.
- miR-31 mimics also led to decreased anti-apoptotic Bcl-2 protein expression and increased apoptosis rates.
- qPCR confirmed significantly higher miR-31 expression in COPD model and miR-31 mimics groups compared to the normal group.
Conclusions:
- Micro ribonucleic acid (miR)-31 activation of the NF-κB signaling pathway aggravates inflammation and apoptosis in rats with chronic obstructive pulmonary disease (COPD).
- These findings suggest that miR-31 may be a potential therapeutic target for managing COPD progression.
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