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Protective Effects of Piceatannol against Selenite-Induced Cataract and Oxidative Damage in Rats
Yating Liu1, Jinglan Li1, Zi Ye1
1Senior Department of Ophthalmology, The Third Medical Center of PLA General Hospital, Beijing, China.
Insights
Piceatannol (PIC) protects against selenite-induced cataracts in rats by reducing lens opacity and improving antioxidant status. This natural compound enhances antioxidant enzyme activity, offering a potential therapeutic strategy for cataract prevention.
Area of Science:
- Biochemistry
- Ophthalmology
- Pharmacology
Background:
- Cataracts are a leading cause of blindness globally, often associated with oxidative stress.
- Selenium compounds can induce cataracts, making them a useful model for studying protective agents.
- Piceatannol, a polyphenol, exhibits antioxidant properties that warrant investigation in ocular health.
Purpose of the Study:
- To evaluate the protective effects of piceatannol against selenite-induced cataracts in Sprague-Dawley rats.
- To explore the therapeutic potential of piceatannol as an antioxidant in preventing cataract formation.
- To investigate the underlying mechanisms of piceatannol's action on oxidative stress markers in the lens.
Main Methods:
- Rats were divided into control, selenite-induced cataract model, and low/high-dose piceatannol treatment groups.
- Cataract induction was achieved via subcutaneous sodium selenite injection.
- Lens opacity, histopathology, oxidative damage indicators (MDA), and antioxidant enzyme activities (GSH, catalase, SOD) were assessed.
- In vitro studies used H2O2-treated SRA01/04 cells with and without piceatannol to assess cell viability and apoptosis.
Main Results:
- Piceatannol treatment significantly reduced lens opacity and histopathological damage compared to the cataract model group.
- Biochemical analysis showed decreased malondialdehyde (MDA) levels and increased antioxidant enzyme activities (GSH, catalase, SOD) in piceatannol-treated rats.
- In vitro, piceatannol effectively restored cell viability and reduced apoptosis in hydrogen peroxide-injured cells.
Conclusions:
- Piceatannol demonstrates significant protective effects against selenite-induced cataracts in a rat model.
- The mechanism involves the upregulation of antioxidant enzyme activity and a reduction in oxidative stress.
- Piceatannol shows promise as a therapeutic agent for preventing or treating cataracts by enhancing the eye's antioxidant defense system.
Purpose:
This study aimed to investigate the protective effects of piceatannol (PIC) on selenite-induced cataracts in Sprague-Dawley rats and explore its therapeutic effects as an antioxidant.
Methods:
Thirty-two eight-day-old rat pups were randomly divided into four groups, with eight pups in each of them. Group 1, as the control group, was injected with the same amount of saline, while Groups 2-4 were administered with sodium selenite (3.46 mg/kg) subcutaneously into the neck on postpartum day 10 for cataract induction. Without further treatment, Group 2 served as the control model, while Groups 3 and 4 (low- and high-dose PIC-treated) had intraperitoneal piceatannol from day 8 to day 17 at doses of 10 mg/kg and 20 mg/kg, respectively. On postpartum day 17, after the last injection, the rat pups were examined for cataract grade by slit lamp, and the lenses of every group were isolated for oxidative damage indicators and further analysis. SRA01/04 cells were exposed to 600 μM H2O2 for 24 hours with or without pretreatment with 10μМ piceatannol. Cell viability was tested by CCK-8 assay and cell apoptosis was evaluated by AnnexinV-PE/7AAD assay.
Results:
This study determined that compared with the model group, the degree of lens opacity was significantly reduced in PIC-treated groups. The histopathological damage of the lenses in the PIC-treated groups improved compared to the model group. There were fewer signs of lesions, such as vacuoles and atrophy. The biochemical results indicated that malondialdehyde (MDA) content of the PIC-treated groups were downregulated and the antioxidant enzyme activities (GSH and catalase) and antioxidant status (SOD) were upregulated compared with the model group. In vitro, piceatannol significantly restored cell viability and cell apoptosis under H2O2 injury.
Conclusion:
Pretreatment with piceatannol may achieve a protective effect on cataract development through upregulating antioxidant enzyme activity.
