Inhibition of inflammation by astaxanthin alleviates cognition deficits in diabetic mice

Zhou, Xiaoyan; Fang, Zhang; Hu, Xiaoru; Chen, Jing; Wen, Xiangru; Sun, Ying; Liu, Yonghai; Tang, Renxian; Zheng, Kuiyang; Song, Yuanjian

doi:10.1016/j.physbeh.2015.08.015

Cited by 83 publications

(44 citation statements)

References 43 publications

(35 reference statements)

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“…The antioxidants, such as grape seed extract and vitamin E were also reported to mitigate hippocampal cell loss in diabetic model [24]. In addition, SFN also possibly ameliorated the memory impairment in diabetic model through anti-inflammation [25]. Recent studies have demonstrated that Nrf2-ARE signaling is also involved in attenuating inflammation-associated pathogenesis [26].…”

Section: Discussionmentioning

confidence: 98%

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

Wang

Fang

Zhen

et al. 2016

Cell Physiol Biochem

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Background/Aims: To explore the effects of sulforaphane (SFN) on neuronal apoptosis in hippocampus and memory impairment in diabetic rats. Methods: Thirty male rats were randomly divided into normal control, diabetic model and SFN treatment groups (N = 10 in each group). Streptozotocin (STZ) was applied to establish diabetic model. Water Morris maze task was applied to test learning and memory. Tunel assaying was used to detect apoptosis in hippocampus. The expressions of Caspase-3 and myeloid cell leukemia 1(MCL-1) were detected by western blotting. Neurotrophic factor levels and AKT/GSK3β pathway were also detected. Results: Compared with normal control, learning and memory were apparently impaired, with up-regulation of Caspase-3 and down-regulation of MCL-1 in diabetic rats. Apoptotic neurons were also found in CA1 region after diabetic modeling. By contrast, SFN treatment prevented the memory impairment, decreased the apoptosis of hippocampal neurons. SFN also attenuated the abnormal expression of Caspase-3 and MCL-1 in diabetic model. Mechanically, SFN treatment reversed diabetic modeling-induced decrease of p-Akt, p-GSK3β, NGF and BDNF expressions. Conclusion: SFN could prevent the memory impairment and apoptosis of hippocampal neurons in diabetic rat. The possible mechanism was related to the regulation of neurotropic factors and Akt/GSK3β pathway.

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Section: Discussionmentioning

confidence: 98%

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

Wang

Fang

Zhen

et al. 2016

Cell Physiol Biochem

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“…A previous study reported that feeding of 0.02% astaxanthin-containing diet for 8 weeks did not affect adult hippocampal neurogenesis in male WT C57BL/6J mice (Yook et al, 2016). Other studies also reported that administration of astaxanthin [80 mg/kg/day, oral gavage for 10 weeks (Yang et al, 2019); 25 mg/kg/day, oral gavage for 10 weeks (4 day/week) (Zhou et al, 2015)] did not affect spatial learning and memory in a Morris water maze test in WT mice. However, a higher dose of astaxanthin (0.5% astaxanthin-containing diet) for 8 weeks enhanced neurogenesis and improved special memory in male WT C57BL/6J mice (Yook et al, 2016).…”

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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“…The marine derived xanthophylls, such as fucoxanthin and astaxanthin, have anti-inflammatory effects and antioxidant activity on different cell lines [56,57]. Furthermore, astaxanthin has also been found to reduce hippocampal and retinal inflammation in streptozotocin-induced diabetic rats, alleviating cognitive deficits, retinal oxidative stress, and depression [17,58,59], while fucoxanthin exerts anti-inflammatory effects against various stimuli through Akt, NF-κB, and mitogen-activated protein kinase pathways [60]. …”

Section: Brain Processes Involved In Neurodegeneration and Protectmentioning

confidence: 99%

On the Neuroprotective Role of Astaxanthin: New Perspectives?

et al. 2018

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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.

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Inhibition of inflammation by astaxanthin alleviates cognition deficits in diabetic mice

Cited by 83 publications

References 43 publications

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

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

On the Neuroprotective Role of Astaxanthin: New Perspectives?

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