Akademik Veri Yönetim Sistemi
TOXICOLOGY AND ENVIRONMENTAL HEALTH SCIENCES, cilt.1, ss.1, 2023 (ESCI)
Abstract
Aim Lung infammation 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. Infammation 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 proinfammatory cytokine levels, and Galectin-3 levels, which modulate cytokine release. Moreover, histopathological
examinations revealed a higher population of difuse lymphocytes and macrophages, indicating increased lung infammation. Dexpanthenol administration ameliorated these adverse efects of nicotine and reduced them to levels comparable to
the control group.
Conclusion Nicotine-induced lung injury promoted oxidative stress and infammation through modulation of NF-κB’s nuclear
translocation. Dexpanthenol, on the other hand, may serve as a dietary supplement to mitigate lung infammation caused by
smoking and tobacco use.
Keywords Nicotine · Dexpanthenol · Lung · NF-κB · Infammation · Oxidative stress