Astaxanthin rescues neuron loss and attenuates oxidative stress induced by amygdala kindling in adult rat hippocampus

Lu, Yan; Xie, Ting; He, Xuexin; Mao, Zhuo-feng; Jia, Lijing; Wei-ping, Wang; Zhen, Junli; Liangmin, Liu

doi:10.1016/j.neulet.2015.04.018

Cited by 38 publications

(31 citation statements)

References 24 publications

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“…In addition, in the amygdala kindling model of epilepsy, AXT lowered seizure activity and reduced neuronal loss in CA3 region of hippocampus of the supplemented rats (Lu et al 2015). These major findings were associated with reduced oxidative damage (MDA and ROS output) and reduced caspase 3 expression with a concomitant decreased release of mitochondrial cytochrome C into cytosol.…”

Section: Therapeutic Potential Of Axt In Neurodegenerative Diseasesmentioning

confidence: 83%

“…This antioxidant versatility is a characteristic of AXT and sets this molecule apart from other carotenoids. Not surprisingly, there is abundant empirical support demonstrating the ability for AXT to reduce ROS in vitro (Liu et al 2009b), and more recent reports have recapitulated these early findings in animal models as described in Table 1. AXT treatment is frequently associated with reduced markers of oxidative damage (Liu et al 2009a;Lu et al 2015;Park et al 2013); however, its mechanisms of action extend far beyond its ability to directly scavenge free radicals. There is significant support that AXT may increase the levels of or promote the activity of endogenous antioxidant enzymes including superoxide dismutase and catalase.…”

Section: Axt Reduces Oxidative Stressmentioning

confidence: 99%

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Neuroprotective mechanisms of astaxanthin: a potential therapeutic role in preserving cognitive function in age and neurodegeneration

et al. 2017

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Astaxanthin (AXT) is a carotenoid with multiple health benefits. It is currently marketed as a health supplement and is well known for its antioxidant capacity. Recent evidence has emerged to suggest a broad range of biological activities. The interest in this compound has increased dramatically over the last few years and many studies are now applying this molecule across many disease models. Results from the current research are beginning to come together to suggest neuroprotective properties including anti-inflammatory, anti-apoptotic, and antioxidant effects, as well as the potential to promote or maintain neural plasticity. These emergent mechanisms of actions implicate AXT as a promising therapeutic agent for neurodegenerative disease. This review will examine and extrapolate from the recent literature to build support for the use of AXT in mitigating neuropathy in normal aging and neurodegenerative disease.

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Section: Therapeutic Potential Of Axt In Neurodegenerative Diseasesmentioning

confidence: 83%

Section: Axt Reduces Oxidative Stressmentioning

confidence: 99%

Neuroprotective mechanisms of astaxanthin: a potential therapeutic role in preserving cognitive function in age and neurodegeneration

et al. 2017

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“…Previous studies showed that ATX, by attenuating oxidative damage, lipid peroxidation, and inhibiting the mitochondrial-related apoptotic pathway, protects hippocampal neurons against epilepsy-induced cellular loss 22 . Additionally, the previous studies reported that ATX prevents inflammation injury and improves cognition in diabetic mice 23 global cerebral ischemia model in rats and also ATX significantly inhibited production of nitric oxide synthase and suppressed oxidative stress process on SH-SY5Y cell line 24 .…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of astaxanthin (ATX) against cognitive impairment on PTZ-induced epileptic seizures in rats and against PTZ-induced neurotoxicity in SH-SY5Y human neuroblastoma cell culture

Karademir

Gümüş

Taştemur

et al. 2019

Cumhuriyet Medical Journal

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Epilepsy is a common brain disorder that seizures could cause neuronal loss in the hippocampus. Oxidative stress has an important role in the pathology of this way. The aim of this study was to investigate the neuroprotective effect of astaxanthin (ATX), on pentylenetetrazole (PTZ) induced epileptic seizures in rats and in SH-SY5Y human neuroblastoma cell culture. Method: In our study, we used 42 male 230-250 g Wistar Albino rats. Animals were divided into seven groups as control, saline (PTZ; 1 ml/kg serum physiologic), positive control (2,5 mg/kg diazepam), 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg ATX for seven days. Thirty min after the administration of the last drug at the indicated doses, PTZ was administered 45 mg/kg to induce an epileptic seizure. The animals were observed for 30 min. Seizure stages according to the Racine Scale (RC) and first myoclonic jerk times (FMJ). Twenty four hours after PTZ injection, passive avoidance test was performed, and then brain tissues were removed for biochemical and histopathological evaluation. The hippocampal Cornu Ammonis 1 (CA1), CA3 and dentate gyrus (DG) regions were evaluated histopathologically regarding neuronal damage. Besides, oxidative stress markers total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) were measured in brain tissues. Furthermore, ATX was performed in vitro SH-SY5Y human neuroblastoma cell culture to evaluate PTZ-induced neurotoxicity. Results: When epileptic behaviors were evaluated, ATX did not affect RC and FMJ (p>0, 05). However, ATX reduced both cognitive impairment in passive avoidance test and neuronal damage in the hippocampus (p<0, 05). Moreover, ATX reduced both TOS levels and OSI in the brain (p<0, 05). Besides of these in vitro studies, ATX increased neuronal viability in vitro. Conclusions: Although ATX does not have antiepileptic properties directly, it has a protective effect on not only in vivo but also in vitro. These effects may occur by possible oxidative pathways.

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“…First, astaxanthin increased the hippocampal PV-positive neuron density in the astaxanthin-fed App NL-G-F mice, which may be attributed to an increase in total GSH in the astaxanthin-fed App NL-G-F mice. Previous studies reported that astaxanthin increased GSH biosynthesis through the nuclear factor erythroidrelated factor 2 and the antioxidant responsive element (Nrf2-ARE) pathway in the rat brain with subarachnoid hemorrhage , and also increased brain GSH levels in other brain disorders due to chemical oxidative stress and amygdalar kindling in rozdents Lu et al, 2015). GSH is an endogenous antioxidant that protects body tissues from oxidative damages, while PV-positive neurons were sensitive to oxidative stress (see Introduction).…”

Section: Protective Mechanisms Of Astaxanthinmentioning

confidence: 99%

Astaxanthin Ameliorated Parvalbumin-Positive Neuron Deficits and Alzheimer’s Disease-Related Pathological Progression in the Hippocampus of AppNL-G-F/NL-G-F Mice

et al. 2020

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Growing evidence suggests that oxidative stress due to amyloid b (Ab) accumulation is involved in Alzheimer's disease (AD) through the formation of amyloid plaque, which leads to hyperphosphorylation of tau, microglial activation, and cognitive deficits. The dysfunction or phenotypic loss of parvalbumin (PV)-positive neurons has been implicated in cognitive deficits. Astaxanthin is one of carotenoids and known as a highly potent antioxidant. We hypothesized that astaxanthin's antioxidant effects may prevent the onset of cognitive deficits in AD by preventing AD pathological processes associated with oxidative stress. In the present study, we investigated the effects of astaxanthin intake on the cognitive and pathological progression of AD in a mouse model of AD. The App NL-G-F/NL-G-F mice were fed with or without astaxanthin from 5-to-6 weeks old, and cognitive functions were evaluated using a Barnes maze test at 6 months old. PV-positive neurons were investigated in the hippocampus. Ab42 deposits, accumulation of microglia, and phosphorylated tau (pTau) were immunohistochemically analyzed in the hippocampus. The hippocampal anti-oxidant status was also investigated. The Barnes maze test indicated that astaxanthin significantly ameliorated memory deficits. Astaxanthin reduced Ab42 deposition and pTau-positive areal fraction, while it increased PVpositive neuron density and microglial accumulation per unit fraction of Ab42 deposition in the hippocampus. Furthermore, astaxanthin increased total glutathione (GSH) levels, although 4-hydroxy-2,3-trans-nonenal (4-HNE) protein adduct levels (oxidative stress marker) remained high in the astaxanthin supplemented mice. The results indicated that astaxanthin ameliorated memory deficits and significantly reversed AD pathological processes (Ab42 deposition, pTau formation, GSH decrease, and PV-positive neuronal

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Astaxanthin rescues neuron loss and attenuates oxidative stress induced by amygdala kindling in adult rat hippocampus

Cited by 38 publications

References 24 publications

Neuroprotective mechanisms of astaxanthin: a potential therapeutic role in preserving cognitive function in age and neurodegeneration

Neuroprotective mechanisms of astaxanthin: a potential therapeutic role in preserving cognitive function in age and neurodegeneration

Neuroprotective effect of astaxanthin (ATX) against cognitive impairment on PTZ-induced epileptic seizures in rats and against PTZ-induced neurotoxicity in SH-SY5Y human neuroblastoma cell culture

Astaxanthin Ameliorated Parvalbumin-Positive Neuron Deficits and Alzheimer’s Disease-Related Pathological Progression in the Hippocampus of AppNL-G-F/NL-G-F Mice

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