Background:
Hydroxytyrosol (HT) is a natural phenolic antioxidant found in olive oil and has been reported to exhibit anti-oxidative and anti-inflammatory bioactivities. However, its potential protective effect in chemically induced retinal injury remains insufficiently defined.
Aim:
This study investigated whether olive oil rich in hydroxytyrosol (OHT) could attenuate sodium iodate (NaIO₃)-induced acute retinal damage in mice.
Methods:
Retinal damage was induced by intraperitoneal injection of 5% NaIO₃ solution at 25 mg/kg body weight. After model establishment, mice received OHT by gavage for 28 consecutive days at 200, 100, or 50 mg/kg. These doses referred to the OHT preparation rather than pure hydroxytyrosol. Serum catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), interleukin-18 (IL-18), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) were measured. Retinal morphology was assessed using paraffin-embedded eye sections, and retinal SERPINF1 and PNPLA2 expression was examined by immunohistochemistry.
Results:
Compared with the model group, OHT treatment increased serum CAT, GSH-Px, and SOD activities and TGF-β levels, while reducing serum MDA, IL-18, and TNF-α levels (P < 0.05 or P < 0.01). Histological observation showed that OHT, particularly at the high dose, partially preserved retinal structure after NaIO₃ exposure. Immunohistochemical analysis further showed higher retinal SERPINF1 and PNPLA2 immunopositive expression in OHT-treated mice than in model mice (P < 0.05 or P < 0.01).
Conclusion:
OHT attenuated NaIO₃-induced retinal damage in mice, possibly through improvement of oxidative stress and inflammatory responses. The concurrent changes in SERPINF1 and PNPLA2 expression suggest that these proteins may be associated with the retinal protective response, although direct mechanistic involvement requires further validation.
Key words: Hydroxytyrosol; Oxidative stress; PNPLA2; Retinal injury; SERPINF1.
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