Protective effects of dexpanthenol against high-fructose corn syrup–induced renal injury: histopathological, oxidative stress, and gene expression analyses in a rat model
Comparative Clinical Pathology, cilt.35, sa.1, 2026 (Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 35 Sayı: 1
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s00580-026-03872-1
- Dergi Adı: Comparative Clinical Pathology
- Derginin Tarandığı İndeksler: Scopus, Zoological Record, Academic Search Ultimate (EBSCO), Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Health Research Premium Collection (ProQuest)
- Anahtar Kelimeler: Aquaporin, Lipid peroxidation, Mitochondrial dysfunction, Renal injury, Tubular degeneration
- Süleyman Demirel Üniversitesi Adresli: Evet
Özet
High-fructose corn syrup (HFCS) consumption may contribute to renal injury through oxidative and cellular stress. This study evaluated the protective effects of dexpanthenol (DEX) against HFCS-induced renal alterations in rats, with particular emphasis on histopathology, oxidative stress, apoptosis-related markers, and selected gene expression changes. Thirty-two male Wistar rats were randomly assigned to Control, HFCS, HFCS + DEX, and DEX groups. (n = 8/group). HFCS was administered in drinking water at 30% for 8 weeks, while DEX was administered intraperitoneally at 500 mg/kg/day during the final 4 weeks. HFCS exposure was associated with renal hyperemia, interstitial hemorrhage, inflammatory cell infiltration, and tubular degeneration together with increased malondialdehyde (MDA) immunoreactivity, total oxidant status (TOS) and oxidative stress index (OSI), and decreased total antioxidant status (TAS). HFCS also increased BAX and decreased Bcl-2 expression (p < 0.001), while mRNA expression of PGC-1α, HO-1, SIRT1, AQP2, and AQP4 was reduced. DEX significantly attenuated histopathological injury, particularly hyperemia and hemorrhage, reduced oxidative stress-related alterations, and improved the BAX/Bcl-2 expression profile. DEX also increased PGC-1α and HO-1 mRNA expression compared with HFCS alone, whereas changes in SIRT1, AQP2, and AQP4 were not statistically significant. Serum creatinine did not differ among groups, despite the observed histopathological and biochemical alterations. Overall, DEX attenuated HFCS-associated renal injury and oxidative stress, whereas HFCS-induced reductions in blood urea nitrogen were not significantly affected by DEX treatment. In conclusion, dexpanthenol attenuated HFCS-associated renal injury and oxidative stress and was associated with changes in selected apoptosis- and antioxidant defense-related markers. These findings support further investigation of DEX as a potential protective agent in HFCS-associated renal injury.