Astaxanthin ameliorates aluminum chloride-induced spatial memory impairment and neuronal oxidative stress in mice

Al-Amin, Md.; Reza, Hasan Mahmud; Saadi, Hasan Mahmud; Mahmud, Waich; Ibrahim, A.; Alam, Musrura Mefta; Kabir, Nadia; Saifullah, Amna; Tropa, Sarjana Tarannum; Quddus, Abdul

doi:10.1016/j.ejphar.2016.02.062

Cited by 67 publications

(47 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[63], and decrease SOD activity in specific brain regions of Swiss albino mice (50 mg/kg/day, 42 days, p.o.) [44]. However, other studies have shown that Al 3+ increases SOD activity in the brain in Swiss albino mice (100 mg/kg/day, 42 days, i.p.)…”

Section: Discussionmentioning

confidence: 91%

See 1 more Smart Citation

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

et al. 2020

View full text Add to dashboard Cite

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al 3+ (7.5 mg/kg/day (0.15 LD 50 ) as AlCl 3 (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl − control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD 50 ), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD 50 ), 21 days, i.g.). The treatment with AlCl 3 increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl 3 treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl 3 treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl 3 had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

show abstract

Section: Discussionmentioning

confidence: 91%

“…However, other studies have indicated that Al 3+ increases GSH levels in all brain regions of Swiss albino mice (50 mg/kg/d, 42 days, per os (p.o.)) [44]. These inconsistencies may be due to differences among animals, dosages, times, experimental conditions, or experimental procedures [45,46].…”

Section: Discussionmentioning

confidence: 99%

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Recent studies reported that ASX could alleviate oxidative stress in vitro and vivo. In human vascular endothelial cells, it would attenuate glucose fluctuation-caused oxidative stress and cell apoptosis [43]; in vivo, ASX was showed to significantly ameliorate hepatic ischemia reperfusion (IR) injury by reducing ROS level and inhibiting MAPK pathway [44]; the underlying mechanism was partly involved with the downregulation of NF-κB activity [45, 46]. The present study demonstrated that ASX treatment markedly inhibited the cobalt toxicity in MG-63 cells, which could be partially attributed to oxidative stress pathway.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin mitigates cobalt cytotoxicity in the MG-63 cells by modulating the oxidative stress

Da-he

Tong

Liu

et al. 2017

BMC Pharmacol Toxicol

View full text Add to dashboard Cite

BackgroundWith the re-popularity of metal-on-metal (MoM) bearing in recent years, the cobalt toxicity has been a cause for concern in the total hip replacement surgery by both physicians and patients.MethodsMG-63 cell line was cultured in vitro and incubated with cobalt (II) chloride (CoCl2) and/or with astaxanthin (ASX) for 24 h. MTT assay was conducted to evaluate the cell viability after cobalt exposure and ASX treatment. Fluorescence-activated cell sorting (FACS) analysis was performed to examine the reactive oxygen species (ROS) level. Quantitative real-time polymerase chain reaction (PCR) was adopted to determine the mRNA levels of related targets. And western blot analysis was used to examine the protein expressions. One-way ANOVA with posttest Newman-Keuls multiple comparisons was adopted to analysis all the obtained data.ResultsIn the current study, ASX exhibited significant protective effect against the Co(II)-induced cytotoxicity in MG-63 cell line. We also found that ASX protected the cells against Co-induced apoptosis by regulating the expression of Bcl-2 family proteins. Besides, heme oxygenase 1 (HO-1) could be activated by Co exposure; ASX treatment significantly inhibited HO-1 activation, suppressing the oxidative stress induced by Co exposure. Moreover, c-Jun N-terminal Kinase (JNK) phosphorylation was shown to participate in the signaling pathway of the protective effect of ASX. However, knockdown of JNK expression by siRNA transfection or JNK inhibitor SP600125 treatment did not affect the protective effect of ASX against cobalt cytotoxicity in MG-63 cells.ConclusionsASX mitigated cobalt cytotoxicity in the MG-63 cells by modulating the oxidative stress. And ASX could be a promising therapy against cobalt toxicity in the hip articulation surgery.Electronic supplementary materialThe online version of this article (doi:10.1186/s40360-017-0166-1) contains supplementary material, which is available to authorized users.

show abstract

“…These findings are in concordance with previously documented effects of aluminium on neuroinflammation and associated spatial memory impairment. 31,32 Administration of Prunus amygdalus nut kernel methanolic extract (0.5mg/kg p.o and 1mg/kg p.o) significantly improved the learning and memory ability as evident by a significant decrease in the transfer latency time in the extract treated groups over a training period of three days (day 10 -day 12). Moreover, there was significant improvement in the retrieval ability of the learned information as evident by a significant increase in the time spent in target quadrant in short term retrieval trials on day 14 as well as on long term retrieval trials on day 22, in contrast to AlCl3 treated group rats.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the protective effect of Prunus amagdylus against aluminium chloride induced neurochemical alterations and spatial memory deficits in rats

Bhatia¹,

Kaur²,

Bhatia³

et al. 2017

Int J Basic Clin Pharmacol

View full text Add to dashboard Cite

Background: The present study was designed to evaluate the protective effect of Prunus amagdylus nut kernels against aluminium chloride induced spatial memory deficits in rats.Methods: Plant material was extracted, and extracts were evaluated for anti-oxidants by DPPH method. Animals were divided into four groups of five animals each. Group 1 was normal group and was kept undisturbed. Group 2 was administered with Aluminium Chloride (4.2mg/kg i.p) for 21 successive days. Group 3 and 4 were pre-administered with Prunus amygdalus methanolic extract at dose 0.5 and 1mg/kg/ p.o) one hour prior to aluminium chloride administration. The memory parameters (both acquisition and retrieval) were evaluated using Morris water maze. After behavioural studies, the animals were sacrificed by decapitation and braintissue thiobarbituric acid reactive substances (TBARS), glutathione (GSH) and catalase activity were measured. Brain tissues from all the groups were histopathologically evaluated using Haematoxylin-eosin staining.Results: Administration of Aluminium chloride resulted in severe memory deficits and neurochemical alterations as was indicated by significant increase in Transfer Latency (TL) time on Morris water maze and increase in the brain tissue TBARS levels in the control group animals. There was significant reduction in the GSH and catalase levels indicating decreased anti-oxidant defence. Histopathologically, control group animal brain tissue showed signs of neuroinflammation. All behavioural and neurochemical and histopathological changes were prevented to a significant extent in the animal groups pre-treated with Prunus amygdalus extract.Conclusions: Methanolic extract of Prunus amaygdalus possesses protective activity against aluminium chloride induced neurotoxicity and associated memory deficits.

show abstract

Astaxanthin ameliorates aluminum chloride-induced spatial memory impairment and neuronal oxidative stress in mice

Cited by 67 publications

References 50 publications

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Natural Compounds Rosmarinic Acid and Carvacrol Counteract Aluminium-Induced Oxidative Stress

Astaxanthin mitigates cobalt cytotoxicity in the MG-63 cells by modulating the oxidative stress

Evaluation of the protective effect of Prunus amagdylus against aluminium chloride induced neurochemical alterations and spatial memory deficits in rats

Contact Info

Product

Resources

About