Protective effect of an astaxanthin nanoemulsion against neomycin-induced hair-cell damage in zebrafish

Takemoto, Yousuke; Hirose, Yoshio; Sugahara, Kazuma; Hashimoto, Makoto; Hara, Hirotaka; Yamashita, Hiroshi

doi:10.1016/j.anl.2017.02.001

Cited by 17 publications

(12 citation statements)

References 20 publications

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“…The otoprotective effects of astaxanthin have been examined in a zebrafish model, although research into its otoprotective effects is limited. 141 Future studies should focus on the pharmaceutical potential and effects of astaxanthin for the treatment of hearing loss, particularly because astaxanthin can be easily absorbed, and when metabolized, it may have greater biological activity than its free form. 3 Future studies should include a therapeutic time window, reliability of drug administration routes, and the optimal dosages of astaxanthin.…”

Section: Resultsmentioning

confidence: 99%

<p>The Role of the Reactive Oxygen Species Scavenger Agent, Astaxanthin, in the Protection of Cisplatin-Treated Patients Against Hearing Loss</p>

Nan¹,

Gu²,

Huang³

2019

DDDT

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Emerging evidence of significant hearing loss occurring shortly after cisplatin administration in cancer patients has stimulated research into the causes and treatment of this side effect. Although the aetiology of cisplatin-induced hearing loss (CIHL) remains unknown, an increasing body of research suggests that it is associated with excessive generation of intracellular reactive oxygen species (ROS) in the cochlea. Astaxanthin, a xanthophyll carotenoid, has powerful anti-oxidant, anti-inflammatory, and anti-apoptotic properties based on its unique cell membrane function, diverse biological activities, and ability to permeate the blood-brain barrier. In this review, we summarize the role of ROS in CIHL and the effect of astaxanthin on inhibiting ROS production. We focus on investigating the mechanism of action of astaxanthin in suppressing excessive production of ROS.

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Section: Resultsmentioning

confidence: 99%

<p>The Role of the Reactive Oxygen Species Scavenger Agent, Astaxanthin, in the Protection of Cisplatin-Treated Patients Against Hearing Loss</p>

Nan¹,

Gu²,

Huang³

2019

DDDT

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“…The mechanism of CDDP-induced ototoxicity is complex and remains unclear. Among possible hypotheses, generation of excessive ROS, such as superoxide radicals, hydrogen peroxide, and hydroxyl radicals, have been implicated as major contributors [31]. Either increased toxic lipid peroxides or depletion of cochlear antioxidant enzyme activities can lead to a cascade resulting in apoptosis of hair cells [2].…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin-loaded polymer-lipid hybrid nanoparticles (ATX-LPN): assessment of potential otoprotective effects

Chen

Tong

et al. 2020

J Nanobiotechnol

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Background: Ototoxicity is one of the major side effects of platinum-based chemotherapy, especially cisplatin therapy. To date, no FDA approved agents to alleviate or prevent this ototoxicity are available. However, ototoxicity is generally believed to be produced by excessive generation of reactive oxygen species (ROS) in the inner ear, thus leading to the development of various antioxidants, which act as otoprotective agents. Astaxanthin (ATX) is an interesting candidate in the development of new therapies for preventing and treating oxidative stress-related pathologies, owing to its unique antioxidant capacity. Methods and results:In this study, we aimed to evaluate the potential antioxidant properties of ATX in the inner ear by using the HEI-OC1 cell line, zebrafish, and guinea pigs. Because ATX has poor solubility and cannot pass through round window membranes (RWM), we established lipid-polymer hybrid nanoparticles (LPN) for loading ATX. The LPN enabled ATX to penetrate RWM and maintain concentrations in the perilymph in the inner ear for 24 h after a single injection. ATX-LPN were found to have favorable biocompatibility and to strongly affect cisplatin-induced generation of ROS, on the basis of DCFHDA staining in HEI-OC1 cells. JC-1 and MitoTracker Green staining suggested that ATX-LPN successfully reversed the decrease in mitochondrial membrane potential induced by cisplatin in vitro and rescued cells from early stages of apoptosis, as demonstrated by FACS stained with Annexin V-FITC/PI. Moreover, ATX-LPN successfully attenuated OHC losses in cultured organ of Corti and animal models (zebrafish and guinea pigs) in vivo. In investigating the protective mechanism of ATX-LPN, we found that ATX-LPN decreased the expression of pro-apoptotic proteins (caspase 3/9 and cytochrome-c) and increased expression of the anti-apoptotic protein Bcl-2. In addition, the activation of JNK induced by CDDP was up-regulated and then decreased after the administration of ATX-LPN, while P38 stayed unchanged. Conclusions:To best of our knowledge, this is first study concluded that ATX-LPN as a new therapeutic agent for the prevention of cisplatin-induced ototoxicity.

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“…As dispersions of small spheroid within an aqueous medium, O/W microemulsions are thermodynamically stable, while nanoemulsions are unstable colloids [134,135]. The bioavailability of AST nanoemulsions has been reported to increase through the elevation of its oxidative and physical stability [136,137]. SLNs are mixtures of O/W nano/microemulsions with the high-ordered inner crystalline structure of lipid phase.…”

Section: Ast Novel Delivery Systems: Nanoformulations Targeted Thmentioning

confidence: 99%

The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective

et al. 2019

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As the leading causes of human disability and mortality, neurological diseases affect millions of people worldwide and are on the rise. Although the general roles of several signaling pathways in the pathogenesis of neurodegenerative disorders have so far been identified, the exact pathophysiology of neuronal disorders and their effective treatments have not yet been precisely elucidated. This requires multi-target treatments, which should simultaneously attenuate neuronal inflammation, oxidative stress, and apoptosis. In this regard, astaxanthin (AST) has gained growing interest as a multi-target pharmacological agent against neurological disorders including Parkinson’s disease (PD), Alzheimer’s disease (AD), brain and spinal cord injuries, neuropathic pain (NP), aging, depression, and autism. The present review highlights the neuroprotective effects of AST mainly based on its anti-inflammatory, antioxidative, and anti-apoptotic properties that underlies its pharmacological mechanisms of action to tackle neurodegeneration. The need to develop novel AST delivery systems, including nanoformulations, targeted therapy, and beyond, is also considered.

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Protective effect of an astaxanthin nanoemulsion against neomycin-induced hair-cell damage in zebrafish

Cited by 17 publications

References 20 publications

<p>The Role of the Reactive Oxygen Species Scavenger Agent, Astaxanthin, in the Protection of Cisplatin-Treated Patients Against Hearing Loss</p>

<p>The Role of the Reactive Oxygen Species Scavenger Agent, Astaxanthin, in the Protection of Cisplatin-Treated Patients Against Hearing Loss</p>

Astaxanthin-loaded polymer-lipid hybrid nanoparticles (ATX-LPN): assessment of potential otoprotective effects

The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective

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