Quinine Attenuates Cigarette Smoke Extract Induced Mucosal Inflammation and Oxidative Stress in the Zebrafish Model

Introduction: Smoking is the primary cause of Chronic obstructive pulmonary disease (COPD) leading to alarming increase in worldwide death. Cigarette smoking is a dangerous risk factor in causing mucosal inflammation and lung damage caused by nicotine, which is more addictive than other narcotics. This study was undertaken to assess the potential of quinine in ameliorating the cigarette smoke extract (CSE) induced inflammation in the Zebrafish model. Materials and Methods: CSE was extracted in water and the Zebrafish was exposed to concentrations ranging from 0.2 to 1.0 cig/L. IC50 of CSE was found to be 0.3 cig/L and this concentration was used for further studies. Induced Zebrafish were treated with 5 mg, 10mg and 15 mg/kg of quinine and analysed for reactive oxygen species, nitric oxide levels, myeloperoxidase activity, histopathology and expression of pro-inflammatory (IL-1) and anti-inflammatory (IL-10) cytokine. Results: The results indicate that exposure of Zebrafish to CSE has significantly increased the levels of ROS, MPO, NO and pro-inflammatory cytokine. Upon treatment with quinine, a dose dependent decrease in these levels was observed with the significantly higher decrease in 15mg/kg treated animals for 8 days. The levels of the anti-inflammatory cytokine, IL-10 tend to be increased with increasing concentration of quinine. The histopathological examination has shown inflammation and damaged gill filaments in the CSE exposed group the Gills inflammation and damaged gill filaments with increased neutrophil accumulation whereas these changes are not observed in the quinine-treated animals. Conclusion: Cumulatively, the results obtained in this study confirm the role of quinine in ameliorating the CSE-induced inflammation in the Zebrafish model.