| Abstrakt: |
Aim: Lung inflammation is a consequence of smoking, tobacco use, nicotine addiction, and the accumulation of toxicants in the body. This study aimed to investigate the association between nicotine-induced lung injury and NF-κB activation, as well as changes in redox balance. Furthermore, the protective role of Dexpanthenol against this damage was examined. Method: A total of 32 male rats were divided into four groups: Control, DEX, Nicotine, and Nicotine + DEX. Nicotine (0.5 mg/kg/day) and Dexpanthenol (500 mg/kg/day) were administered intraperitoneally. Subsequently, the levels of nuclear and cytoplasmic NF-κB in lung tissue were analyzed. Inflammation and oxidative stress markers and histopathological evaluations of the lung tissue were conducted. Results: Nicotine administration resulted in increased levels of tissue MDA and TOS, as well as decreased levels of GSH-Px, GSH, GST, SOD, and TAS. Additionally, nicotine administration led to elevated nuclear expression of NF-κB protein, IL-1β, IL-6 proinflammatory cytokine levels, and Galectin-3 levels, which modulate cytokine release. Moreover, histopathological examinations revealed a higher population of diffuse lymphocytes and macrophages, indicating increased lung inflammation. Dexpanthenol administration ameliorated these adverse effects of nicotine and reduced them to levels comparable to the control group. Conclusion: Nicotine-induced lung injury promoted oxidative stress and inflammation through modulation of NF-κB's nuclear translocation. Dexpanthenol, on the other hand, may serve as a dietary supplement to mitigate lung inflammation caused by smoking and tobacco use. [ABSTRACT FROM AUTHOR] |
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