The protective effect of astaxanthin on learning and memory deficits and oxidative stress in a mouse model of repeated cerebral ischemia/reperfusion

Xue, Yan; Qu, Zhenzhen; Fu, Junfen; Zhen, Junli; Wang, Wenjing; Cai, Yunlei; Wang, Weiping

doi:10.1016/j.brainresbull.2017.04.019

Cited by 64 publications

(38 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Stroke is a leading cause of disability in adults, resulting in social and economic burdens worldwide [81,82]. Numerous attempts [1,2,13,[83][84][85][86][87][88][89][90][91][92][93][94] have been made to reveal the pathological mechanisms underlying cerebral ischemia and to design new drugs [2,[95][96][97][98][99] that reduce the effects of complications due to stroke [100][101][102]. Because all of the pharmacological interventions that have been tested to date have failed, new targets for novel therapies are needed.…”

Section: Discussionmentioning

confidence: 99%

Roles Played by the Na+/Ca2+ Exchanger and Hypothermia in the Prevention of Ischemia-Induced Carrier-Mediated Efflux of Catecholamines into the Extracellular Space: Implications for Stroke Therapy

et al. 2019

View full text Add to dashboard Cite

The release of [ 3 H]dopamine ([ 3 H]DA) and [ 3 H]noradrenaline ([ 3 H]NA) in acutely perfused rat striatal and cortical slice preparations was measured at 37 °C and 17 °C under ischemic conditions. The ischemia was simulated by the removal of oxygen and glucose from the Krebs solution. At 37 °C, resting release rates in response to ischemia were increased; in contrast, at 17 °C, resting release rates were significantly reduced, or resting release was completely prevented. The removal of extracellular Ca 2+ further increased the release rates of [ 3 H]DA and [ 3 H]NA induced by ischemic conditions. This finding indicated that the Na + /Ca 2+ exchanger (NCX), working in reverse in the absence of extracellular Ca 2+ , fails to trigger the influx of Ca 2+ in exchange for Na + and fails to counteract ischemia by further increasing the intracellular Na + concentration ([Na + ] i ). KB-R7943, an inhibitor of NCX, significantly reduced the cytoplasmic resting release rate of catecholamines under ischemic conditions and under conditions where Ca 2+ was removed. Hypothermia inhibited the excessive release of [ 3 H] DA in response to ischemia, even in the absence of Ca 2+ . These findings further indicate that the NCX plays an important role in maintaining a high [Na + ] i , a condition that may lead to the reversal of monoamine transporter functions; this effect consequently leads to the excessive cytoplasmic tonic release of monoamines and the reversal of the NCX. Using HPLC combined with scintillation spectrometry, hypothermia, which enhances the stimulation-evoked release of DA, was found to inhibit the efflux of toxic DA metabolites, such as 3,4-dihydroxyphenylacetaldehyde (DOPAL). In slices prepared from human cortical brain tissue removed during elective neurosurgery, the uptake and release values for [ 3 H]NA did not differ from those measured at 37 °C in slices that were previously maintained under hypoxic conditions at 8 °C for 20 h. This result indicates that hypothermia preserves the functions of the transport and release mechanisms, even under hypoxic conditions. Oxidative stress (H 2 O 2 ), a mediator of ischemic brain injury enhanced the striatal resting release of [ 3 H]DA and its toxic metabolites (DOPAL, quinone). The study supports our earlier findings that during ischemia transmitters are released from the cytoplasm. In addition, the major findings of this study that hypothermia of brain slice preparations prevents the extracellular calcium concentration ([Ca 2+ ] o )-independent non-vesicular transmitter release induced by ischemic insults, inhibiting Na + /Cl − -dependent membrane transport of monoamines and their toxic metabolites into the extracellular space, where they can exert toxic effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Roles Played by the Na+/Ca2+ Exchanger and Hypothermia in the Prevention of Ischemia-Induced Carrier-Mediated Efflux of Catecholamines into the Extracellular Space: Implications for Stroke Therapy

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Xue and co-authors [35] evaluated the efficacy of AST treatment after repeated cerebral IR injury in a mouse model. These researchers demonstrated that astaxanthin improved learning and decreased memory impairment and neuronal damage.…”

Section: Astaxanthin Against Cerebral Ischemia/reperfusion (Ir)mentioning

confidence: 99%

“…Moreover, astaxanthin treatment reduced oxidative stress, restoring GHS levels and SOD activity, and significantly suppressed the concentration of MDA. Xue and co-authors [35] also highlighted a decrease in protein expression of cytochrome C (Cyt C) and caspase-3 (cleaved Caspase-3), both involved in the occurrence and development of apoptosis.…”

Section: Astaxanthin Against Cerebral Ischemia/reperfusion (Ir)mentioning

confidence: 99%

On the Neuroprotective Role of Astaxanthin: New Perspectives?

et al. 2018

View full text Add to dashboard Cite

Astaxanthin is a carotenoid with powerful antioxidant and anti-inflammatory activity produced by several freshwater and marine microorganisms, including bacteria, yeast, fungi, and microalgae. Due to its deep red-orange color it confers a reddish hue to the flesh of salmon, shrimps, lobsters, and crayfish that feed on astaxanthin-producing organisms, which helps protect their immune system and increase their fertility. From the nutritional point of view, astaxanthin is considered one of the strongest antioxidants in nature, due to its high scavenging potential of free radicals in the human body. Recently, astaxanthin is also receiving attention for its effect on the prevention or co-treatment of neurological pathologies, including Alzheimer and Parkinson diseases. In this review, we focus on the neuroprotective properties of astaxanthin and explore the underlying mechanisms to counteract neurological diseases, mainly based on its capability to cross the blood-brain barrier and its oxidative, anti-inflammatory, and anti-apoptotic properties.

show abstract

“…By reducingoxidative stress, astaxanthin has been shown to protect neuronal cells from reactive oxygen species-mediate toxicity [20], and decrease ischemia/reperfusion-induced hippocampal pyramidal neuron loss and learning and memory deficits [21]. Astaxanthin has also been shown to inhibit aluminum-induced activation of glial cells and generation of reactive oxygen species, consequently improving the spatial memory and locomotor activity in aluminum-treated animals [22].…”

Section: Astaxanthin and Neurodegenerative Diseasesmentioning

confidence: 99%