Akademik Veri Yönetim Sistemi
The Journal of craniofacial surgery, 2025 (SCI-Expanded, Scopus)
Objectives: This study aims to investigate the protective effects of melatonin in particulate matter (PM2.5)-induced lung damage. Methods: Fourteen adult male Wistar albino rats were used in the research. The animals were randomly assigned to either the PM2.5 control group (n = 7) or the research group (n = 7) that also received melatonin. In distilled water, the control and experimental groups were given 100 mg/kg of PM2.5 intratracheally every 4 weeks. Melatonin (20 mg/kg/day) was delivered intraperitoneally to the experimental group for 30 days. The histologic evaluation included looking for bleeding, vascular congestion, cellular infiltration, and bronchiolar wall epithelial cell sloughing. Results: The authors’ study demonstrated that the PM2.5 + melatonin group had considerably lower levels of all examined parameters than the PM2.5 group. These metrics included epithelial cell sloughing in the bronchiolar wall, bleeding, vascular congestion, and cellular infiltration in the interalveolar region. Lung light microscopy in the PM2.5 group reveals extensive cellular inflammation, most noticeably in the interalveolar spaces, the bronchiolar lumen, and the peribronchiolar and perivascular regions. Bronchiolar epithelium sloughing, bleeding, and vascular congestion are further symptoms. The histologic appearance of the alveolar structures’ thin walls is near normal, and there is less inflammation and damage in the PM2.5 + melatonin group. Conclusion: Melatonin may protect the lungs from PM2.5-induced damage by activating the Nrf2/HO-1 signaling pathway and reducing iNOS and TNF-α production. When applied to lung epithelial cells, melatonin inhibits EMT and lessens fibrosis. To further understand how melatonin protects individuals PM2.5-induced lung injury, the authors suggest conducting more human trials.