Histopathology and NF-κB/Caspase-3 Expression in High Fructose Corn Syrup– Induced Lung Injury: Protective Effect of Dexpanthenol
Duzce Medical Journal, cilt.28, sa.2, ss.118-125, 2026 (ESCI, Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 28 Sayı: 2
- Basım Tarihi: 2026
- Doi Numarası: 10.18678/dtfd.1843989
- Dergi Adı: Duzce Medical Journal
- Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, CINAHL, EMBASE, Directory of Open Access Journals, TR DİZİN (ULAKBİM), Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO)
- Sayfa Sayıları: ss.118-125
- Anahtar Kelimeler: apoptosis, dexpanthenol, fibrosis, High fructose corn syrup, inflammation, lung injury
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
Aim: High-fructose corn syrup (HFCS) has been associated with metabolic and inflammatory disturbances, including pulmonary inflammatory injury. Due to its known anti-inflammatory and tissue-protective properties, this study aimed to investigate the protective effects of dexpanthenol (DEXP) against HFCS-induced structural and molecular lung damage in rat lungs. Material and Methods: Thirty-two male Wistar rats were allocated at random into four groups (Control, HFCS, HFCS+DEXP, DEXP). HFCS (30%) was provided in drinking water for 8 weeks. DEXP was administered intraperitoneally at a dose of 500 mg/kg/day for the last 2 weeks. Lung tissues were processed for hematoxylin–eosin and Picro Sirius Red staining. Hyperemia, edema, epithelial loss, inflammatory cell infiltration, and fibrosis were evaluated semi-quantitatively. The immunohistochemical expression of NF-κB and Caspase-3 was assessed as markers of inflammatory and apoptotic activities. Results: Exposure to HFCS produced alterations such as thickened alveolar walls, interstitial edema, vascular hyperemia, degeneration and loss of epithelial cells, accumulation of inflammatory cells, and early deposition of collagen compared with the control group. Histopathological scores for inflammation, edema, hyperemia, epithelial loss, and fibrosis were significantly increased in the HFCS group (p=0.001, p=0.001, p=0.001, p=0.006, and p=0.011, respectively). In addition, NF-κB and Caspase-3 expression levels were significantly elevated in the HFCS group compared with the control group (p=0.001). DEXP treatment significantly reduced histopathological scores (p=0.001), as well as NF-κB and Caspase-3 expression levels compared with the HFCS group (p=0.001 and p=0.0018, respectively). In the DEXP-only group, lung morphology was preserved. Conclusion: Chronic ingestion of HFCS elicits prominent inflammatory, apoptotic, and fibrotic responses in rat lung tissue. DEXP exerts strong histoprotective and immunomodulatory actions, suggesting potential therapeutic value against HFCS-induced pulmonary injury.