Protective Effect of Althaea officinalis on Nicotine-Induced Lung Injury
Acta Cytologica, ss.1, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1159/000553245
- Dergi Adı: Acta Cytologica
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CINAHL, EMBASE, MEDLINE
- Sayfa Sayıları: ss.1
- Anahtar Kelimeler: Althaea officinalis, Althaea officinalis, Althaea officinalis, Herbal medicine, Lung injury, Lungenschädigung, Lésion pulmonaire, Nicotine, Nicotine, Nikotin, Oxidative stress, Oxidativer Stress, Phytotherapie, Phytothérapie, Stress oxydatif
- Yozgat Bozok Üniversitesi Adresli: Evet
Özet
Introduction: Nicotine contributes to chronic pulmonary diseases by promoting oxidative stress, inflammation, and tissue remodeling, leading to alveolar destruction, septal thickening, and fibrosis. Althaea officinalis (AO), a medicinal plant with antioxidant and anti-inflammatory properties, may counteract these effects; however, its protective role against nicotine-induced lung injury is not well characterized. This study aimed to evaluate the impact of AO on nicotine-related oxidative and histological lung damage in rats. Methods: Thirty-two female Wistar albino rats were divided into four groups: control, AO (250 mg/kg), nicotine (0.5 mg/kg), and AO + nicotine. Treatments were administered for 14 days. Lung tissues were collected for biochemical and histopathological analyses. Oxidative stress was assessed by measuring superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels. Lung injury was evaluated using hematoxylin-eosin and Masson’s trichrome staining, while apoptosis was assessed by Bax immunostaining. Results: Nicotine exposure increased MDA levels, Bax expression, and histological damage, while reducing SOD activity. AO co-treatment significantly reversed these effects by lowering MDA levels, reducing Bax immunoreactivity, restoring SOD activity, and improving lung architecture, including reduced alveolar destruction and septal thickening (p < 0.05). Conclusion: AO demonstrated notable antioxidant and cytoprotective effects against nicotine-induced lung injury. Its ability to reduce oxidative stress, apoptosis, and tissue damage suggests therapeutic potential for preventing pulmonary oxidative injury, supporting further research for possible clinical application.