Cyanidin-3-glucoside inhibits glutamate-induced Zn2+ signaling and neuronal cell death in cultured rat hippocampal neurons by inhibiting Ca2+-induced mitochondrial depolarization and formation of reactive oxygen species

Yang, Ji Seon; Perveen, Shazia; Ha, Tae Joung; Kim, Seong Yun; Yoon, Shin Hee

doi:10.1016/j.brainres.2015.02.028

Cited by 22 publications

(26 citation statements)

References 50 publications

(56 reference statements)

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“…In this study, we demonstrated that GCD was diminished by cyanidin. Likely, oral administration of morin, a bio lavonoid 1 day before the KA injection, and then administered for 7 more days markedly reduced the KAinduced GCD in the hippocampus by reducing oxidative stress (Yang et al, 2015).…”

Section: Alterations In Reactive Astrocytesmentioning

confidence: 89%

“…The study reported that cyanidin-3glucoside (C3G), which is also in the anthocyanin family showed the effect to prevent neuronal death from ischemia condition (Bhuiyan et al, 2012). Moreover, C3G can prevent neuronal death in the rat hippocampus by inhibiting Ca 2+ induced mitochondrial dysfunction and reducing the formation of ROS (Yang et al, 2015). In Alzheimer's disease, C3G plays a role to protect cell death from the accumulation of beta-amyloid-induced ROS formation (Song et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Thongrong

Kongsui

Sriraksa

2020

ijrps

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Temporal lobe epilepsy (TLE) is one of the non-communicable diseases characterized by dentate granule cell dispersion (GCD) and the loss of the CA1 and CA3 neurons. This study investigated the effects of cyanidin on neurodegeneration after KA injection. Male Wistar rats were divided into a saline-injected group as a control, KA alone and cyanidin treated group at a dose of 10 mg/kg BW seven days before and after KA injection. The histomorphological analysis revealed that GCD was reduced in the ipsilateral hippocampus of cyanidin treated group when compared with KA alone (P<0.05). There was no neurodegeneration observed in the contralateral hippocampus. In contrast, neuronal degeneration was limited in the ipsilateral CA1 (P<0.01) and the hilar interneurons (P<0.001) of cyanidin treated group when compared with KA alone. However, there was no significant difference in the number of CA3 neurons of the ipsilateral between KA alone and cyanidin treated group. GFAP staining revealed a higher number of reactive astrocytes in the ipsilateral hilus (P<0.001) and molecular layer (P<0.05) of cyanidin treated group when compared with KA alone. Taken together, cyanidin could prevent neurodegeneration and promote astrocyte proliferation as well as mitigated GCD following KA-induced hippocampal injury.

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Section: Alterations In Reactive Astrocytesmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Thongrong

Kongsui

Sriraksa

2020

ijrps

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“…Isolations of rat hippocampal cells were grown in primary coculture as previously described with minor modifications [ 9 ]. Primary cells were obtained from the hippocampi of embryonic day 17 adult maternal Sprague-Dawley rats (250–300 g).…”

Section: Methodsmentioning

confidence: 99%

“…Flavonoids have been known to inhibit various ion channels, including Ca 2+ -permeable ion channels [ 7 8 9 ]. Cyanidin-3-glucoside (C3G), a component of anthocyanin, belongs to the flavonoid family.…”

Section: Introductionmentioning

confidence: 99%

“…Cyanidin-3-glucoside (C3G), a component of anthocyanin, belongs to the flavonoid family. C3G has been reported to exert a neuroprotective effect against glutamate-induced neuronal cell death in cultured hippocampal neurons [ 9 ] as well as in vitro ischemia-induced neuronal cell death [ 10 ], in vivo ischemia-induced neuronal cell death [ 11 ], ethanol neurotoxicity in the developing brain [ 12 ], and Aβ-induced cell death in cell line [ 13 14 ]. However, little is known about how C3G affects Aβ-induced neuronal cell death in cultured rat hippocampal neurons.…”

Section: Introductionmentioning

confidence: 99%

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Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons

Yang

Jeon

Yoon

et al. 2018

Korean J Physiol Pharmacol

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Increasing evidence implicates changes in [Ca2+]i and oxidative stress as causative factors in amyloid beta (Aβ)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting Ca2+ and Zn2+ signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ25–35-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for Ca2+, Zn2+, MMP and ROS. Treatment with Aβ25–35 (20 µM) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited Aβ25–35-induced [Zn2+]i increases as well as [Ca2+]i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ25–35-induced mitochondrial depolarization. C3G also blocked the Aβ25–35-induced formation of ROS. In addition, C3G significantly inhibited the Aβ25–35-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid β-induced neuronal cell death by reducing multiple apoptotic signals.

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Cyanidin: Advances on Resources, Biosynthetic Pathway, Bioavailability, Bioactivity, and Pharmacology

Forsan,

Awad

2023

Handbook of Dietary Flavonoids

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Cyanidin-3-glucoside inhibits glutamate-induced Zn2+ signaling and neuronal cell death in cultured rat hippocampal neurons by inhibiting Ca2+-induced mitochondrial depolarization and formation of reactive oxygen species

Cited by 22 publications

References 50 publications

Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons

Cyanidin: Advances on Resources, Biosynthetic Pathway, Bioavailability, Bioactivity, and Pharmacology

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Cyanidin-3-glucoside inhibits glutamate-induced Zn2+ signaling and neuronal cell death in cultured rat hippocampal neurons by inhibiting Ca2+-induced mitochondrial depolarization and formation of reactive oxygen species

Cited by 22 publications

References 50 publications

Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Cyanidin prevents hippocampal cell death and promotes astrocytosis in kainic acid-induced neurodegeneration

Cyanidin-3-glucoside inhibits amyloid β25–35-induced neuronal cell death in cultured rat hippocampal neurons

Cyanidin: Advances on Resources, Biosynthetic Pathway, Bioavailability, Bioactivity, and Pharmacology

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Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons