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Fig 6. Effect of AST and lutein on ICAM-1, MCP-1, and FKN expression in aqueous humors. Aqueous humor was isolated and pooled from the eyes of rats by each group. ICAM-1, MCP-1, and FKN levels were quantified by 3 repeat ELISA experiments. Data are presen
Figure 9. Fig 6. Effect of AST and lutein on ICAM-1, MCP-1, and FKN expression in aqueous humors. Aqueous humor was isolated and pooled from the eyes of rats by each group. ICAM-1, MCP-1, and FKN levels were quantified by 3 repeat ELISA experiments. Data are presented as the mean ± SD. *, p < 0.05 versus the Control group; #, p < 0.05 versus the Diabetes group.

Deskripsi

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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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 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.

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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.

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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 9

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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 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.](https://pdfs.citedhealth.com/figures/26765843/288.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/)
<figure>
  <img src="https://pdfs.citedhealth.com/figures/26765843/288.png" alt="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." />
  <figcaption>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.<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>
</figure>

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Astaxanthin untuk Oxidative Stress

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