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Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
Published on: February 10, 2012
Effects of Nicotine administration on α7nAChR, miR-124, STAT3, and inflammatory markers in Rat Lung Tissue
Narges Dastmalchi1, Fatemeh Asaadi1, Elham Karimi-Sales1,2
1Stem Cell Research Center, Tabriz University of Medical Sciences, Golgasht St, Tabriz, Iran.
Background:
Nicotine, the major alkaloid in tobacco, interacts with nicotinic acetylcholine receptors (nAChRs), particularly α7nAChR, which is involved in inflammatory regulation. MicroRNA‑124 (miR‑124) and signal transducer and activator of transcription 3 (STAT3) also participate in inflammatory signaling. This study investigated the effects of nicotine on α7nAChR, miR‑124, phosphorylated STAT3 (p‑STAT3), MCP‑1, and IL‑10 expression in rat lung tissue.
Methods:
Adult male Wistar rats (n = 8/group) received different doses of nicotine. Lung tissues were collected for molecular analyses. Expression of α7nAChR and miR‑124 was assessed using quantitative real‑time PCR (qRT‑PCR). Protein levels of α7nAChR and p‑STAT3 were evaluated by Western blotting, and MCP‑1 and IL‑10 levels were measured using ELISA.
Results:
Nicotine exposure was associated with a dose‑dependent increase in α7nAChR expression. miR‑124 expression increased at the lower nicotine dose but decreased at higher doses. Alterations in p‑STAT3 protein levels were also observed following nicotine administration. MCP‑1 levels decreased at the lower dose and increased at higher doses, whereas IL‑10 levels increased in nicotine‑treated groups.
Conclusion:
Nicotine administration was associated with changes in α7nAChR, miR‑124, p‑STAT3, MCP‑1, and IL‑10 expression in rat lung tissue, suggesting a potential association between nicotine exposure and inflammatory signaling pathways in the lung.
