Effects of Nicotine Administration on the Expression Levels of alpha7 Nicotinic Acetylcholine Receptor, miRNA-124, STAT3, and Inflammatory Factors in Lung Tissue

Background Nicotine, a major alkaloid in tobacco, interacts with nicotinic acetylcholine receptors (nAChRs), notably alpha7 nAChR, which are key modulators of inflammatory signaling. The α7nAChR regulates the release of pro-inflammatory cytokines, a process modulated by microRNA-124 (miR-124), which downregulates inflammatory mediators. Additionally, STAT3, a transcription factor activated by cytokines, is inhibited by miR-124. This study aimed to evaluate the effects of nicotine on the expression of α7nAChR, miRNA-124, STAT3 protein, and inflammatory cytokines (IL-10 and MCP-1) in rat lung tissue. Methods Adult male Wistar rats were treated with varying doses of nicotine. Lung tissues were collected for molecular analysis. Gene expression levels were examined using qRT-PCR, while protein levels were assessed through Western blotting. Cytokine concentrations were measured with ELISA kits. Results Nicotine exposure led to a dose-dependent increase in α7nAChR mRNA and protein expression. Elevated nicotine levels significantly enhanced STAT3 protein and altered the expression of miRNA-124. ELISA results showed changes in inflammatory (MCP-1) and anti-inflammatory (IL-10) cytokine levels. Statistical analysis confirmed the significance at (p < 0.05). Conclusion Nicotine modulates both inflammatory and anti-inflammatory signaling pathways in rat lung tissue, suggesting a dual regulatory role through α7nAChR and associated molecular mediators. This interaction between α7-nAChR, miR-124, and STAT3 forms a crucial signaling pathway linking cholinergic activity to neuroinflammation regulation, suggesting potential therapeutic targets for neurodegenerative diseases driven by inflammation and neuronal injury.