Astaxanthin protects against kainic acid-induced seizures and pathological consequences

Chang, Yi; Lu, Cheng Wei; Chen, Yi Jing; Lin, Tzu-Yu; Huang, Shu Kuei; Wang, Su‐Jane

doi:10.1016/j.neuint.2018.02.008

Cited by 17 publications

(12 citation statements)

References 58 publications

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“…KBA, at the doses of 10 and 50 mg/kg, administrated (i. p.) 30 min prior to KA reduced KA-induced neuronal death in the CA3 region compared with KA only. On the other hand, in agreement with previously published data [32,33], a significant elevation of glutamate levels in the hippocampus was observed at 4 h after KA administration (i. p.) (p < 0.001) (▶ Fig. 6 b).…”

Section: Resultssupporting

confidence: 92%

“…6, KBA exerts a neuroprotective effect in a rat model of excitotoxicity induced by KA administration (15 mg/kg, i. p.). KA is a nonselective agonist of KA and ionotropic glutamate receptors, and its administration to animals results in selective neuronal death in specific brain regions, especially in the hippocampal CA3 region [33,38], which has the highest density of KA receptors [39]. KA-induced neuronal death is associated with the pathological release of glutamate [40,41].…”

Section: Discussionmentioning

confidence: 99%

“…KA was dissolved in 0.9 % NaCl (pH 7.0), at a dose of 15 mg/kg, and was injected (i. p.). The dose of administration was chosen based on previous experiments of our group and others [32,33,38]. KBA dissolved in 1 % DMSO was administered i. p. for 30 min prior to KA injection.…”

Section: In Vivo Studiesmentioning

confidence: 99%

“…Glutamate concentration was measured from dissected hippocampus tissues as described previously [32,33]. Briefly, animals were sacrificed through decapitation and the brains were removed immediately.…”

Section: Determination Of Glutamate By High-performance Liquid Chromamentioning

confidence: 99%

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11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus

Lin

Wang

2020

Planta Med

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Excessive glutamate concentration induces neuronal death in acute brain injuries and chronic neurodegenerative diseases. Natural compounds from medicinal plants have attracted considerable attention for their use in the prevention and treatment of neurological disorders. 11-Keto-β-boswellic acid, a triterpenoid found in the medicinal plant Boswellia serrata, has neuroprotective potential. The present study investigated the effect of 11-keto-β-boswellic acid on glutamate release in vitro and kainic acid-induced glutamate excitotoxicity in vivo in the rat hippocampus. In rat hippocampal nerve terminals (synaptosomes), 11-keto-β-boswellic acid dose-dependently inhibited 4-aminopyridine-stimulated glutamate release. This effect was dependent on extracellular calcium, persisted in the presence of the glutamate transporter inhibitor DL-threo-β-benzyloxyaspartate, and was blocked by the vesicular transporter inhibitor bafilomycin A1. In addition, 11-keto-β-boswellic acid reduced the 4-aminopyridine-induced increase in intrasynaptosomal Ca2+ levels. The N- and P/Q-type channel blocker ω-conotoxin MVIIC and the protein kinase A inhibitor H89 significantly suppressed the 11-keto-β-boswellic acid-mediated inhibition of glutamate release, whereas the intracellular Ca2+-releasing inhibitors dantrolene, CGP37157, and xestospongin C, mitogen-activated protein kinase inhibitor PD98059, as well as protein kinase C inhibitor calphostin C had no effect. In a rat model of excitotoxicity induced by intraperitoneal kainic acid injection (15 mg/kg), intraperitoneal 11-keto-β-boswellic acid administration (10 or 50 mg/kg) 30 min before kainic acid injection considerably ameliorated kainic acid-induced glutamate concentration elevation and CA3 neuronal death. These data suggested that 11-keto-β-boswellic acid inhibits glutamate release from the rat hippocampal synaptosomes by suppressing N- and P/Q-type Ca2+ channels and protein kinase A activity, as well as exerts protective effects against kainic acid-induced excitotoxicity in vivo.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: In Vivo Studiesmentioning

confidence: 99%

Section: Determination Of Glutamate By High-performance Liquid Chromamentioning

confidence: 99%

See 2 more Smart Citations

11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus

Lin

Wang

2020

Planta Med

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“…Neuronal preservation by Astaxanthin under stress conditions manifested by upregulation of, e.g., cAMP response element-binding protein (CREB) or brain-derived neurotrophic factor (BDNF) was also demonstrated in vitro ( 99 ). Glutamate-related excitotoxicity has been prevented by Astaxanthin pre-treatment in rats ( 100 ), possibly, through inhibiting endoplasmic reticulum stress caused by calcium influx ( 101 ).…”

Section: Discussionmentioning

confidence: 99%

Cognitive Effects of Astaxanthin Pretreatment on Recovery From Traumatic Brain Injury

et al. 2020

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Traumatic brain injury (TBI), caused by mechanical impact to the brain, is a leading cause of death and disability among young adults, with slow and often incomplete recovery. Preemptive treatment strategies may increase the injury resilience of high-risk populations such as soldiers and athletes. In this work, the xanthophyll carotenoid Astaxanthin was examined as a potential nutritional preconditioning method in mice (sabra strain) to increase their resilience prior to TBI in a closed head injury (CHI) model. The effect of Astaxanthin pretreatment on heat shock protein (HSP) dynamics and functional outcome after CHI was explored by gavage or free eating (in pellet form) for 2 weeks before CHI. Assessment of neuromotor function by the neurological severity score (NSS) revealed significant improvement in the Astaxanthin gavage-treated group (100 mg/kg, ATX) during recovery compared to the gavage-treated olive oil group (OIL), beginning at 24 h post-CHI and lasting throughout 28 days ( p < 0.007). Astaxanthin pretreatment in pellet form produced a smaller improvement in NSS vs. posttreatment at 7 days post-CHI ( p < 0.05). Cognitive and behavioral evaluation using the novel object recognition test (ORT) and the Y Maze test revealed an advantage for Astaxanthin administration via free eating vs. standard chow during recovery post-CHI (ORT at 3 days, p < 0.035; improvement in Y Maze score from 2 to 29 days, p < 0.02). HSP profile and anxiety (open field test) were not significantly affected by Astaxanthin. In conclusion, astaxanthin pretreatment may contribute to improved recovery post-TBI in mice and is influenced by the form of administration.

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Mechanism of cell death pathways in status epilepticus and related therapeutic agents

Du¹,

He²,

Zhao³

et al. 2022

Biomedicine & Pharmacotherapy

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Astaxanthin protects against kainic acid-induced seizures and pathological consequences

Cited by 17 publications

References 58 publications

11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus

11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus

Cognitive Effects of Astaxanthin Pretreatment on Recovery From Traumatic Brain Injury

Mechanism of cell death pathways in status epilepticus and related therapeutic agents

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