Astaxanthine Research Articles

Astaxanthin protects against hearing impairment in diabetic rats

ObjectiveDiabetes Mellitus (DM) causes an increase in oxidative stress that leads to deterioration in auditory functions. Astaxanthine (AST) is known to have strong antioxidant effects. In this study, the aim is to investigate the effect of AST against hearing loss that is due to DM. MethodsThis study is an experimental animal study. The study was designed in four groups with 8 animals (n = 8) in each group. The groups were as follows; Control Group (CNT), Diabetic Group (DM), AST applied diabetic group (DM+AST), and AST applied non-diabetic group (AST). Streptozotocin was applied in rats to induce DM. AST was administered by oral gavage. Auditory Brainstem Responses (ABR) and Distortion Product Otoacoustic Emissions (DPOAE) tests were performed on several days of the study. At the end of the study, pro-inflammatory cytokine levels were analyzed in cochlear tissue samples, and Glutathione Peroxidase (GPx), Superoxide Dismutase (SOD), Catalase (CAT) and Malondialdehyde (MDA) levels were measured. ResultsWhen the findings obtained in the ABR and DPOAE tests in the DM group, it was observed that there was a significant deterioration in the hearing sense. This deterioration was not observed in the DM+AST group. In the DM group, GPx, SOD and CAT levels decreased and MDA levels increased in blood and cochlear tissue. Compared to the DM group, it was noted that antioxidant enzyme levels increased and MDA levels decreased in the DM+AST group. Cochlear tissue pro-inflammatory cytokine levels, which increased with DM, were significantly decreased in the DM+AST group. ConclusionEven though the effects of AST were investigated in a diabetic experimental animal model, if this molecule is proven to be effective in diabetic humans, it can be considered an adjunct therapeutic option with its antioxidant effects. Level of evidenceThe level of evidence of this article is 5. This article is an experimental animal and laboratory study.

Astaxanthine attenuates cisplatin ototoxicity in vitro and protects against cisplatin-induced hearing loss in vivo

Astaxanthine (AST) has important biological activities including antioxidant and anti-inflammatory effects that could alleviate neurological and heart diseases, but its role in the prevention of cisplatin-induced hearing loss (CIHL) is not yet well understood. In our study, a steady interaction between AST and the E3 ligase adapter Kelch-like ECH-associated protein 1, a predominant repressor of nuclear factor erythroid 2-related factor 2 (NRF2), was performed and tested via computer molecular docking and dynamics. AST protected against cisplatin-induced ototoxicity via NRF2 mediated pathway using quantitative PCR and Western blotting. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential revealed that AST reduced ROS overexpression and mitochondrial dysfunction. Moreover, AST exerted anti-apoptosis effects in mouse cochlear explants using immunofluorescence staining and HEI-OC1 cell lines using quantitative PCR and Western blotting. Finally, AST combined with poloxamer was injected into the middle ear through the tympanum, and the protection against CIHL was evaluated using the acoustic brain stem test and immunofluorescent staining in adult mice. Our results suggest that AST reduced ROS overexpression, mitochondrial dysfunction, and apoptosis via NRF2-mediated pathway in cisplatin-exposed HEI-OC1 cell lines and mouse cochlear explants, finally promoting cell survival. Our study demonstrates that AST is a candidate therapeutic agent for CIHL.

The influence of dietary antioxidant on ovarian eggs and levels of vitamin E, C, A, astaxanthin, β-carotene and oxidative stres in tissues of Astacus leptodactylus (Eschscholtz) during reproduction

The experiment was conducted to determine the most effective antioxidant (among the vitamin E (VE), vitamin C (VC), vitamin A (VA), astaxanthine (AX), β-carotene (βC)) on the ovarian egg number and size, level of VE, VC, VA, AX, βC and oxidative stress (as malondialdehyde (MDA)) in the hepatopancreas, ovarian, gills and muscle tissue during ovarian development of Astacus leptodactylus. One control (C) and five experimental diets (EE, EC, EA, EAX and EβC) were prepared. The EE, EC, EA, EAX and EβC groups were formed by added 150 mg kg-1 VE, 200 mg kg-1 VC, 240 mg kg-1 VA, 200 mg kg-1 AX and 200 mg kg-1 βC to diet C, respectively. At the end of the experiment found that the dietary antioxidants increased ovarian egg number and size and reduced the level of MDA in the tissues. Ovarian egg number and size were highest in the EE and EAX diet groups in the comparison to control (p<0.001). The level of MDA in the tissues was lowest in the EAX diet group in the comparison to control (p<0.001). The highest levels of VE, VC, VA, AX and βC were found in the hepatopancreas and ovarian compared with muscle and gills. The highest level of MDA also was determined in the ovarian according to other tissues. In conclusion, the VE and AX in broodstock diets were the most effective antioxidants on the ovarian egg number and size of A. leptodactylus.

Astaxanthine Secured Apoptotic Death of PC12 Cells Induced by β-Amyloid Peptide 25–35: Its Molecular Action Targets

Astaxanthine (ASTx) is a novel carotenoid nutraceutical occurring in many crustaceans and red yeasts. It has potent antioxidant, photoprotective, hepatodetoxicant, and anti-inflammatory activities. Documented effect of ASTx on treatment of neurodegenerative disease is still lacking. We used the beta-amyloid peptide (Abeta) 25-35-treated PC12 model to investigate the neuron-protective effect of ASTx. The parameters examined included cell viability, caspase activation, and various apoptotic biomarkers that play their critical roles in the transduction pathways independently or synergistically. Results indicated that Abeta25-35 at 30 microM suppressed cell viability by 55%, whereas ASTx was totally nontoxic below a dose of 5.00 microM. ASTx at 0.1 microM protected PC12 cells from damaging effects of Abeta25-35 in several ways: (1) by securing the cell viability; (2) by partially down-regulating the activation of caspase 3; (3) by inhibiting the expression of Bax; (4) by completely eliminating the elevation of interleukin-1beta and tumor necrosis factor-alpha; (5) by inhibiting the nuclear translocation of nuclear factor kappaB; (6) by completely suppressing the phosphorylation of p38 mitogen-activated protein kinase; (7) by completely abolishing the calcium ion influx to effectively maintain calcium homeostasis; and (8) by suppressing the majority (about 75%) of reactive oxygen species production. Conclusively, ASTx may have merit to be used as a very potential neuron protectant and an anti-early-stage Alzheimer's disease adjuvant therapy.