Emine SARMAN, Halil AŞÇI, İrem NAZİROĞLU, Öznur KOLAY, Esra ŞİRAZİ
Anatolian Current Medical Journal - 2026;8(4):645-651
Aims: This study aimed to investigate the potential protective effects of agomelatine (AGO) against lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats, with a focus on histopathological alterations and immunohistochemical markers of apoptosis and inflammation. Methods: A total of 32 adult female Wistar rats were randomly assigned to four groups: Control, LPS, LPS+AGO and AGO. LPS (5 mg/kg) was administered intraperitoneally to induce ALI, followed by oral AGO (20 mg/kg) treatment in the LPS+AGO group. Lung tissue samples were examined histopathologically using Hematoxylin-Eosin staining to assess edema, detachment/disruption of bronchiolar epithelium, disorganization of bronchiolar smooth muscle and thickening of the alveolar epithelium. Apoptotic and inflammatory responses were evaluated immunohistochemically via Caspase 3 (Cas-3) and tumor necrosis factor alpha (TNF-alpha) expression. Results: LPS administration induced significant histopathological alterations, including interstitial edema, epithelial detachment, smooth muscle disorganization and alveolar wall thickening (p<0.01 for edema, p<0.001 for all the other parameters vs. control). Cas-3 and TNF-alpha immunoreactivity were markedly elevated in the LPS group (p<0.001), predominantly in alveolar and bronchiolar epithelial regions. AGO treatment significantly reduced all histopathological injury scores and attenuated Cas-3 and TNF-alpha expression (p<0.001 vs. LPS), preserving normal lung architecture and reducing apoptotic and inflammatory responses. Conclusion: AGO exerts protective effects against LPS-induced lung injury by mitigating histopathological damage, associated with reduced apoptotic and inflammatory markers. These findings suggest that AGO may have potential therapeutic value in experimental sepsis-related ALI and warrant further investigation.
