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. 2024 Nov 19;25(1):411.
doi: 10.1186/s12931-024-03042-3.

Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking

Juanjuan Xiong  1 , Li Xie  2 , YiRan Huang  2 , JiaHui Zhu  2 , ZhiYan Hong  2 , HaoYun Qian  2 , Jingjing Liu  2
Affiliations

Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking

Juanjuan Xiong et al. Respir Res. .

Abstract

Background: Passive smoke has a significant impact on lung function and constitutes a critical public health issue, as smoking generates free radicals that damage the lungs and other tissues. Currently, limited research exists on whether the antioxidant melatonin can mitigate lung damage caused by smoking. This study aims to investigate the mechanisms through which melatonin alleviates acute lung disease induced by passive smoking.

Methods: Rats were divided into five groups (n = 6): a control group and three groups exposed to low, medium, and high concentrations of smoke, and a melatonin treatment group.

Results: Data indicated that in the high concentration passive smoking group, the alveolar structure of the lung tissue was destroyed, and the total antioxidant capacity in lung tissue diminished as the concentration of smoke increased. The expressions of TNF-α, IL-6, and IL-1β exhibited similar results. The anti-apoptotic factors Bcl-2 and Bcl-xL mRNA level significantly decreased in the high concentration smoking group, while no significant changes were observed in the medium and low concentration groups. Conversely, the high concentration passive smoking increased the pro-apoptotic factors Bax and Caspase-3 mRNA levels. Additionally, endogenous melatonin levels in lung tissue gradually decreased following exposure to smoke, whereas the exogenous melatonin alleviated the changes in inflammatory factors and apoptosis-related factors in lung tissue. Furthermore, at high smoking concentrations, the mRNA levels of lung cancer-related genes vascular endothelial growth factor (VEGF), cytochromeP450 1A1 (CYP1A1), and cytochrome P450 1B1 (CYP1B1) were significantly increased, while exogenous melatonin reduced the expression of these genes in lung tissue.

Conclusions: These findings suggest that melatonin can diminish lung tissue damage, apoptosis, and inflammatory responses induced by passive smoking, as well as decrease the expression of lung cancer-related genes. Further experimental investigations involving exogenous melatonin treatments will be needed.

Keywords: Lung; Melatonin; Oxidative stress; Passive smoking.

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Conflict of interest statement

Declarations Ethics approval and consent to participate The study was approved by the Ethics Committee of Jinling Institute of Technology. Consent for publication Not applicable. Competing interests The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Melatonin concentration in rat lung tissue. Different letters on the column indicate significant differences (P < 0.05) between treatment groups. Statistical significance was assessed using analysis of variance (ANOVA) followed by a multiple comparison test with Dunnett adjustment
Fig. 2
Fig. 2
Hematoxylin eosin (HE) staining shows alveolar damage caused by cigarette smoke in rats. A: control group; B: low concentration passive smoking group; C: high concentration passive smoking group; D: melatonin treatment group. Scale bar = 100 μm
Fig. 3
Fig. 3
Melatonin alleviates oxidative stress induced by passive smoking in rat lung. A: Total antioxidant capacity; B: Tumor necrosis factor alpha (TNF-α); C: Interleukin 6 (IL-6). D: Interleukin 1 beta (IL-1β). Different letters on the column indicate significant differences (P < 0.05) between treatment groups. Statistical significance was assessed using analysis of variance (ANOVA) followed by a multiple comparison test with Dunnett adjustment
Fig. 4
Fig. 4
Melatonin alleviates passive smoking-induced apoptotic genes in rat lung tissue. A: mRNA level of anti-apoptotic factor Bcl-2; B: mRNA level of anti-apoptotic factor Bcl-xl; C: mRNA level of pro-apoptotic factor Bax; D: mRNA level of pro-apoptotic factor Caspase-3. Different letters on the column indicate significant differences (P < 0.05) between treatment groups. Statistical significance was assessed using analysis of variance (ANOVA) followed by a multiple comparison test with Dunnett adjustment
Fig. 5
Fig. 5
Melatonin alleviates the effect of passive smoking on oncogenes in rat lung tissue. A: mRNA level of vascular endothelial growth factor (VEGF); B: mRNA level of cytochrome P4501A1 (CYP1A1); C: mRNA level of Cytochrome P4501B1 (CYP1B1); Different letters on the column indicate significant differences (P < 0.05) between treatment groups. Statistical significance was assessed using analysis of variance (ANOVA) followed by a multiple comparison test with Dunnett adjustment
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