Figure 4

Electroretinography (ERG) recordings evaluating retinal function in control and STZ-induced diabetic rats treated with normal saline, 0.6 mg/kg AST, 3 mg/kg AST, or 0.5 mg/kg lutein for 8 weeks. ERG wave amplitudes indicate the functional impact of each treatment on diabetic retinal physiology.

Figure 5

Inflammatory marker expression levels in retinal tissue or aqueous humor of diabetic rats, comparing astaxanthin-treated groups with untreated diabetic controls. Results indicate AST may modulate inflammatory mediator production.

Figure 6

Western blot or protein expression analysis of retinal inflammatory and oxidative stress markers in the diabetic rat model, demonstrating the molecular effects of astaxanthin treatment on key signaling proteins.

Figure 7

Gene or protein expression data for retinal vascular endothelial growth factor (VEGF) or related angiogenic markers in AST-treated versus untreated diabetic rats.

Figure 9

Quantification of ICAM-1, MCP-1, and fractalkine (FKN) protein levels in aqueous humor of diabetic rats treated with astaxanthin or lutein. Reduced expression of these inflammatory mediators suggests AST may attenuate vascular inflammation in diabetic eyes.

Figure 10

Supplementary analysis of inflammatory or oxidative markers in ocular tissues of STZ-induced diabetic rats, providing additional evidence for astaxanthin's protective mechanism against diabetic retinal damage.