Effects of astaxanthin on antioxidation in human aqueous humor

Hashimoto, Hirotaka; Arai, Katsumi; Hayashi, Shimmin; Okamoto, Hiroyuki; Takahashi, Jun; Chikuda, Makoto; Obara, Yoshitaka

doi:10.3164/jcbn.13-6

Cited by 35 publications

(21 citation statements)

References 17 publications

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“…Oral administration of AST reportedly increased the AST levels in the anterior chamber, resulting in an increase in antioxidant potential. 44 Thus, it may be possible that AST injected into the air chamber of a chicken egg and uptaken into the blood could have passed through a barrier into the eye, having exerted antioxidant actions. But, it is not clear whether AST acted in the eye, since AST levels were not determined in the eye in this study.…”

Section: Figurementioning

confidence: 99%

Effect of Astaxanthin on Cataract Formation Induced by Glucocorticoids in the Chick Embryo

Ishikawa

Hashizume

Nishigori

et al. 2014

Current Eye Research

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Section: Figurementioning

confidence: 99%

Effect of Astaxanthin on Cataract Formation Induced by Glucocorticoids in the Chick Embryo

Ishikawa

Hashizume

Nishigori

et al. 2014

Current Eye Research

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“…Furthermore, astaxanthin attenuates RGC death under various stresses in a murine model [17]. Oral supplementation of astaxanthin is also reported to enhance superoxide scavenging activity in human aqueous humor [20].…”

Section: Introductionmentioning

confidence: 95%

Haematococcus pluvialis-Derived Astaxanthin Is a Potential Neuroprotective Agent against Optic Nerve Ischemia

Lin

Kapupara²,

Wen³

et al. 2020

Marine Drugs

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Astaxanthin, a xanthophyll belonging to the family of carotenoids, is a potent antioxidant. However, much less is known about its protective effects on the oxidative stress of ischemic optic nerve. We hypothesized that astaxanthin treatment could protect retinal ganglion cells (RGCs) from death via anti-oxidative and anti-apoptotic responses. Adult male Wistar rats were fed astaxanthin (100 mg/kg/day) by daily gavage for seven consecutive days, either before or after inducing oxidative stress in the retina by photodynamic treatment. The visual function, RGC apoptosis, macrophage infiltration in the optic nerve, expression of p-Akt, p-mTOR, SGK1, pS6K, Nrf2, p62, TNFα, Il1β in retinas were investigated. The visual function and the RGC densities were significantly higher in both pre- and post-treatment groups. The numbers of apoptotic RGCs and extrinsic macrophage infiltration in the optic nerve were significantly decreased in both astaxanthin-treated groups. Furthermore, pre- and post-treatment of astaxanthin showed a higher expression of p-Akt, p-mTOR, Nrf2 and superoxide dismutase activity, and a lower expression of cleaved caspase-3, suggesting anti-apoptotic and anti-oxidative roles. Our findings indicate that astaxanthin can preserve visual function and reduce RGC apoptosis after ischemic insults. Including astaxanthin in daily diet as a supplement may be beneficiary for ischemic optic neuropathy.

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“…Furthermore, AST decreases retinal oxidative stress in streptozotocin-induced diabetes [16], reduces retinal ischemia damage [17], and inhibits cell death of retinal ganglion cells under various stresses [18] in murine models. In humans, AST oral supplementation is reported to increase superoxide scavenging activity of aqueous humor [19]. …”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Oral Astaxanthin Nanopowder against Ultraviolet‐Induced Photokeratitis in Mice

Harada

Morikawa

Lennikov

et al. 2017

Oxidative Medicine and Cellular Longevity

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Purpose Astaxanthin (AST) has a strong antioxidant cellular membrane chaperone protective effect. Recently, a water-soluble nanosized AST (nano-AST) form was produced, which is expected to improve the efficacy of oral intake effects. The purpose of this study was to examine whether oral nano-AST has therapeutic effects on UV-induced photokeratitis in mice. Methods C57BL/6 mice were administered twice with either nano-AST, AST oil, lutein, or bilberry extracts 3 hours before and shortly before UV irradiation (dose: 400 mJ/cm2). The corneas were collected 24 hours after irradiation and stained with H&E and TUNEL. NF-κB, dihydroethidium (DHE), COX-2, p-IκB-α, TNFα, and CD45 expression were evaluated through immunohistochemistry, Western blot analysis, and qPCR. Results Corneal epithelium was significantly thicker in mice orally administered with nano-AST than in the others (p < 0.01), with significantly less NF-κB nucleus translocation (p < 0.001), and significantly fewer TUNEL cells (p < 0.01). Weaker DHE signals were detected in the nano-AST group (p < 0.05) relative to the others. Furthermore, reduced inflammation and decreased cell death in corneal tissue were observed in the nano-AST group, as indicated by a reduction in the expression of COX-2, p-IκB-α, TNFα, and CD45. Conclusions Oral administration of nano-AST demonstrated a protective effect on UV-induced photokeratitis via antioxidative, anti-inflammatory, and antiapoptotic activity.

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Effects of astaxanthin on antioxidation in human aqueous humor

Cited by 35 publications

References 17 publications

Effect of Astaxanthin on Cataract Formation Induced by Glucocorticoids in the Chick Embryo

Effect of Astaxanthin on Cataract Formation Induced by Glucocorticoids in the Chick Embryo

Haematococcus pluvialis-Derived Astaxanthin Is a Potential Neuroprotective Agent against Optic Nerve Ischemia

Protective Effects of Oral Astaxanthin Nanopowder against Ultraviolet‐Induced Photokeratitis in Mice

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