مقالات پذیرفته شده در نهمین کنگره بین المللی زیست پزشکی
The protective effects of nicotine, with and without blockade of peroxisome proliferator-activated receptor gamma (PPARγ), on lung injury induced by saline lavage in rats
The protective effects of nicotine, with and without blockade of peroxisome proliferator-activated receptor gamma (PPARγ), on lung injury induced by saline lavage in rats
Hossein fatemikia,1,*Farzaneh Ketabchi,2
1. Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran 2. Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
Introduction: Our previous research demonstrated that nicotine, an α7 nicotinic acetylcholine receptor (α7nAChR) agonist, reduces inflammation and acute lung injury in a saline lavage-induced rat model. This study investigates the mechanistic role of PPAR-γ activation in mediating nicotine’s protective effects.
Methods: Male rats were divided into five groups: Sham, saline lavage (LAV), LAV treated with nicotine (LAV+NIC), LAV treated with a PPAR-γ antagonist BAG (LAV+BAG), and LAV treated with BAG and NIC (LAV+BAG+NIC). After tracheostomy and femoral catheterization, lung injury was induced by 10 repeated saline lavages (30 mL saline at 37°C). The recovery phase lasted for 3 hours, and drugs were injected 1 hour after the last lavage.
Results: Nicotine improved mean blood pressure, heart rate, airway pressures, and lung compliance through α7nAChR even in the presence of BAG in the LAV+BAG+NIC group. However, plasma and lung tissue malondialdehyde (MDA) in the LAV+BAG+NIC group were higher than in the Sham and LAV+NIC groups. Furthermore, in the LAV+BAG+NIC group, the neutrophil percentage in bronchoalveolar lavage (BAL) was higher, and the macrophage percentage was lower than those in the Sham and LAV+NIC groups.
Conclusion: In this study, we did not detect any interaction between PPAR-γ receptors and α7nAChR receptors in hemodynamic and lung compliance data. Nevertheless, PPAR-γ receptors could interfere with the effects of the α7nAChR agonist nicotine on inflammation, oxidative stress, as well as gas exchange. These results indicate that nicotine’s protective effects are partially mediated through PPAR-γ receptors.