Astaxanthin: A mechanistic review on its biological activities and health benefits

Fakhri, Sajad; Abbaszadeh, Fatemeh; Dargahi, Leila; Jorjani, Masoumeh

doi:10.1016/j.phrs.2018.08.012

Cited by 308 publications

(203 citation statements)

References 232 publications

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“…Astaxanthin (ATX) belongs to the xanthophyll group and has a great reputation for its outstanding antioxidant capacity to neutralize free radicals and balance prooxidant and antioxidant [12]. Currently, accumulating evidences also prove that ATX has multiple beneficial effects, such as antiinflammation, antiapoptosis, and antiobesity activities [13]. Importantly, ATX has been suggested to reduce blood pressure and prevent vascular remodeling in SHRs [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Chen

Guo

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress aggravates mitochondrial injuries and accelerates the proliferation of vascular smooth muscle cells (VSMCs), which are important mechanisms contributing to vascular remodeling in hypertension. We put forward the hypothesis that Astaxanthin (ATX), known to possess strong features of antioxidant, could attenuate vascular remodeling by inhibiting VSMC proliferation and improving mitochondrial function. The potential effects of ATX were tested on spontaneously hypertensive rats (SHRs) and cultured VSMCs that injured by angiotensin II (Ang II). The results showed that ATX lowered blood pressure, reduced aortic wall thickness and fibrosis, and decreased the level of reactive oxygen species (ROS) and H 2 O 2 in tunica media. Moreover, ATX decreased the expression of proliferating cell nuclear antigen (PCNA) and ki67 in aortic VSMCs. In vitro, ATX mitigated VSMC proliferation and migration, decreased the level of cellular ROS, and balanced the activities of ROSrelated enzymes including NADPH oxidase, xanthine oxidase, and superoxide dismutase (SOD). Besides, ATX mitigated Ca 2+ overload, the overproduction of mitochondrial ROS (mtROS), mitochondrial dysfunction, mitochondrial fission, and Drp1 phosphorylation at Ser616. In addition, ATX enhanced mitophagy and mitochondrial biosynthesis by increasing the expression of PINK, parkin, mtDNA, mitochondrial transcription factor A (Tfam), and PGC-1α. The present study indicated that ATX could efficiently treat vascular remodeling through restraining VSMC proliferation and restoring mitochondrial function. Inhibiting mitochondrial fission by decreasing the phosphorylation of Drp1 and stimulating mitochondrial autophagy and biosynthesis via increasing the expression of PINK, parkin, Tfam, and PGC-1α may be part of its underlying mechanisms.

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Section: Introductionmentioning

confidence: 99%

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Chen

Guo

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…In the present study, AST treatment prevented blood glucose alteration in SCI rats. AST has currently gained attention as a beneficial natural oral agent for the management of diabetes (Fakhri, Abbaszadeh, Darghahi & Jorjani, 2018;Liu et al, 2013;Otton et al, 2010). AST enhances insulin-stimulated glucose transporter-4 translocation to the plasma membrane, promotes the IRS-PI3K-Akt pathway (Bhuvaneswari & Anuradha, 2012), modulates peroxisome proliferator-activated receptor gamma (PPAR-γ) and therefore reduces insulin resistance (Inoue et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Effects of astaxanthin on sensory‐motor function in a compression model of spinal cord injury: Involvement of ERK and AKT signalling pathway

Fakhri

Dargahi

Abbaszadeh

et al. 2018

European Journal of Pain

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Background Spinal cord injury (SCI) causes continuous neurological deficits and major sensory‐motor impairments. There is no effective treatment to enhance sensory‐motor function following SCI. Thus, it is crucial to develop novel therapeutics for this particular patient population. Astaxanthin (AST) is a strong antioxidant, anti‐inflammatory and anti‐apoptotic agent. In the present study, it was tested in a severe compression SCI model with emphasis on sensory‐motor outcomes, signalling pathway, along with other complications. Methods A severe SCI was induced by compression of the rat thoracic spinal cord with an aneurysm clip and treatment with AST or the vehicle was carried out, 30 min after injury. Behavioural tests including open field, von Frey, hot plate and BBB were performed weekly to 28 days post‐injury. Rats were assigned to measure blood glucose, weight and auricle temperature. Western blot and histological analysis also were performed at the same time points. Results AST decreased mechanical and thermal pain and also improved motor function performance, reduced blood glucose and auricle temperature increases and attenuated weight loss in SCI rats. Western blot analysis showed decreased activation of ERK1/2 and increased activation of AKT following AST treatment. The histology results revealed that AST considerably preserved myelinated white matter and the number of motor neurons following SCI. Conclusion Taken together, the beneficial effects of AST to improve sensory‐motor outcomes, attenuate pathological tissue damage and modulate ERK and AKT signalling pathways following SCI, suggest it as a strong therapeutic agent towards clinical applications. Significance Spinal cord injury (SCI) impairs sensory‐motor function and causes complications, which astaxanthin (AST) has the potential to be used as a treatment for. The present study investigates the effects of AST in a compression model of SCI with emphasis on sensory‐motor outcomes alongside other complications, histopathological damage and also related signalling pathways.

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“…The antioxidative property of dietary ASTX has been widely reported in both terrestrial and aquatic animals (Fakhria, Abbaszadeh, Dargahi, & Jorjani, ; Sefc, Brown, & Clotfelter, ; Shimidza, Goto, & Miki, ; Zuluaga, Gueguen, Letourneur, & Pavon‐Djavid, ). However, less information has been available about the effects of ASTX on the antioxidative status of fish intestine.…”

Section: Introductionmentioning

confidence: 99%

The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer Takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota

Liao

et al. 2018

Aquacult Nutr

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A 74‐day feeding trial was conducted to evaluate the effects of dietary astaxanthin (ASTX) on antioxidative status, inflammatory response and microbiota in the intestine of tiger puffer. Four diets differed only in ASTX content, that is, 0 (Control), 50 (ASTX50), 100 (ASTX100) and 500 (ASTX500) mg/kg. Compared with Control, ASTX50 and ASTX100 significantly reduced the malondialdehyde content and spared the activities of antioxidative enzymes in hindgut; however, ASTX500 had higher activity and gene expression of antioxidative enzymes. Nuclear factor‐erythroid 2 p45‐related factor 2 (Nrf2) and Kelch‐like ECH‐associated protein 1 (Keap1) signalling were probably involved in the transcriptional regulation of antioxidative enzymes by dietary ASTX. Compared with Control and ASTX500, ASTX50 and ASTX100 decreased the leucocyte infiltration in the lamina propria of hindgut and down‐regulated the gene expression of tumour necrosis factor‐α (TNF‐α) and interleukin‐8 (IL‐8). ASTX markedly affected the overall structure of intestinal microbiota. The relative abundance of Arcobacter, which has harmful properties, was the lowest in ASTX100 but the highest in ASTX500. In conclusion, dietary ASTX at 50 or 100 mg/kg improved the antioxidative status, alleviated the inflammation and favourably modulated the microbiota in tiger puffer intestine, but excess ASTX exerted contrary effects.

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Astaxanthin: A mechanistic review on its biological activities and health benefits

Cited by 308 publications

References 232 publications

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Effects of astaxanthin on sensory‐motor function in a compression model of spinal cord injury: Involvement of ERK and AKT signalling pathway

The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer Takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota

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