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Fig 1. Evaluation of functional changes of the retina by electroretinography (ERG). The ERG were performed on untreated rats (Control) or STZinduced diabetic rats treated for 8 weeks with normal saline (Diabetes), 3 mg/kg AST (AST High), 0.6 mg/kg AST (AS
Figure 4. Fig 1. Evaluation of functional changes of the retina by electroretinography (ERG). The ERG were performed on untreated rats (Control) or STZinduced diabetic rats treated for 8 weeks with normal saline (Diabetes), 3 mg/kg AST (AST High), 0.6 mg/kg AST (AST Low), or 0.5 mg/kg lutein (Lutein). The relative b-wave ratio was significantly decreased in the Diabetes, AST Low and Lutein groups compared with the Control group. The relative b-wave ratio in AST High group had no significant difference from Control group. The ratio in AST High group was significantly higher than that in the AST Low and the Lutein groups (p = 0.046 and p < 0.001). The data are expressed as the mean ± SD in 4 rats for each group (bar graph). *, p < 0.05 compared with the control group. #, p < 0.05 compared with the Diabetes group. Differences among groups were analyzed by one-way analysis of variance followed by Bonferroni’s test for multiple comparisons.

Deskripsi

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.

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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 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.

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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 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.

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

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.

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Histological or immunohistochemical analysis of retinal tissue sections from diabetic rats, comparing structural changes across treatment groups to assess astaxanthin's protective effects on retinal architecture.

Figure 8

Histological or immunohistochemical analysis of retinal tissue sections from diabetic rats, comparing structural changes across treatment groups to assess astaxanthin's protective effects on retinal architecture.

micrograph
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 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.

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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.

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.

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Figure 4

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Source Paper

Astaxanthin Inhibits Expression of Retinal Oxidative Stress and Inflammatory Mediators in Streptozotocin-Induced Diabetic Rats.

PloS one (2016)

PMID: 26765843

DOI: 10.1371/journal.pone.0146438

Cite This Figure

![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.](https://pdfs.citedhealth.com/figures/26765843/235.png)

> Source: Po-Ting Yeh et al. "Astaxanthin Inhibits Expression of Retinal Oxidative Stress and Inflammatory Med." *PloS one*, 2016. PMID: [26765843](https://pubmed.ncbi.nlm.nih.gov/26765843/)
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  <img src="https://pdfs.citedhealth.com/figures/26765843/235.png" alt="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." />
  <figcaption>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.<br>  Source: Po-Ting Yeh et al. "Astaxanthin Inhibits Expression of Retinal Oxidative Stress and Inflammatory Med." <em>PloS one</em>, 2016. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/26765843/">26765843</a></figcaption>
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Astaxanthin untuk Oxidative Stress

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