Cassia obtusifolia seed ameliorates amyloid β-induced synaptic dysfunction through anti-inflammatory and Akt/GSK-3β pathways

Tea infused with the seed of Cassia obtusifolia has been traditionally used as an herbal remedy for liver, eye, and acute inflammatory diseases. Recent pharmacological reports have indicated that Cassiae semen has neuroprotective effects, attributable to its anti-inflammatory actions, in ischemic st...

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Veröffentlicht in:Journal of ethnopharmacology 2016-02, Vol.178, p.50-57
Hauptverfasser: Yi, Jee Hyun, Park, Hey Jin, Lee, Seungheon, Jung, Ji Wook, Kim, Byeong C., Lee, Young Choon, Ryu, Jong Hoon, Kim, Dong Hyun
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container_end_page 57
container_issue
container_start_page 50
container_title Journal of ethnopharmacology
container_volume 178
creator Yi, Jee Hyun
Park, Hey Jin
Lee, Seungheon
Jung, Ji Wook
Kim, Byeong C.
Lee, Young Choon
Ryu, Jong Hoon
Kim, Dong Hyun
description Tea infused with the seed of Cassia obtusifolia has been traditionally used as an herbal remedy for liver, eye, and acute inflammatory diseases. Recent pharmacological reports have indicated that Cassiae semen has neuroprotective effects, attributable to its anti-inflammatory actions, in ischemic stroke and Parkinson's disease models. Previously, the ethanol extract of C. obtusifolia seeds (COE) was reported to have memory enhancing properties. However, the effects of COE in an Alzheimer's disease (AD) model are currently unknown. In this study, we investigated the effect(s) of COE on aberrant synaptic plasticity and memory impairment induced by amyloid β (Aβ), a key toxic component found in the AD brain. To determine the effect of COE on Aβ-induced aberrant synaptic plasticity, we used acute mouse hippocampal slices and delivered theta burst stimulation to induce long-term potentiation (LTP). Western blots were used to detect Aβ- and/or COE-induced changes in signaling proteins. The novel object location recognition test was conducted to determine the effect of COE on Aβ-induced recognition memory impairment. COE was found to ameliorate Aβ-induced LTP impairment in the acute hippocampal slices. Glycogen synthase kinase-3β (GSK-3β), a key molecule in LTP impairment, was activated by Aβ. However, this process was inhibited by COE via Akt signaling. Moreover, COE was found to attenuate Aβ-induced microglia, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX) activation. In the in vivo studies performed, COE ameliorated the Aβ-induced object recognition memory impairment. These results suggest that COE exhibits neuroprotective activities against Aβ-induced brain disorders. [Display omitted]
doi_str_mv 10.1016/j.jep.2015.12.007
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Recent pharmacological reports have indicated that Cassiae semen has neuroprotective effects, attributable to its anti-inflammatory actions, in ischemic stroke and Parkinson's disease models. Previously, the ethanol extract of C. obtusifolia seeds (COE) was reported to have memory enhancing properties. However, the effects of COE in an Alzheimer's disease (AD) model are currently unknown. In this study, we investigated the effect(s) of COE on aberrant synaptic plasticity and memory impairment induced by amyloid β (Aβ), a key toxic component found in the AD brain. To determine the effect of COE on Aβ-induced aberrant synaptic plasticity, we used acute mouse hippocampal slices and delivered theta burst stimulation to induce long-term potentiation (LTP). Western blots were used to detect Aβ- and/or COE-induced changes in signaling proteins. The novel object location recognition test was conducted to determine the effect of COE on Aβ-induced recognition memory impairment. COE was found to ameliorate Aβ-induced LTP impairment in the acute hippocampal slices. Glycogen synthase kinase-3β (GSK-3β), a key molecule in LTP impairment, was activated by Aβ. However, this process was inhibited by COE via Akt signaling. Moreover, COE was found to attenuate Aβ-induced microglia, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX) activation. In the in vivo studies performed, COE ameliorated the Aβ-induced object recognition memory impairment. These results suggest that COE exhibits neuroprotective activities against Aβ-induced brain disorders. 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COE was found to ameliorate Aβ-induced LTP impairment in the acute hippocampal slices. Glycogen synthase kinase-3β (GSK-3β), a key molecule in LTP impairment, was activated by Aβ. However, this process was inhibited by COE via Akt signaling. Moreover, COE was found to attenuate Aβ-induced microglia, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX) activation. In the in vivo studies performed, COE ameliorated the Aβ-induced object recognition memory impairment. These results suggest that COE exhibits neuroprotective activities against Aβ-induced brain disorders. 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subjects Alzheimer Disease - drug therapy
Alzheimer Disease - metabolism
Amyloid beta
Amyloid beta-Peptides - metabolism
Animals
Anti-Inflammatory Agents - chemistry
Anti-Inflammatory Agents - pharmacology
Cassia - chemistry
Cassia obtusifolia
Cassia obtusifolia seeds
Chromosome Pairing - drug effects
Glycogen Synthase Kinase 3 - metabolism
Glycogen Synthase Kinase 3 beta
Hippocampus - drug effects
Hippocampus - metabolism
Long-term potentiation
Long-Term Potentiation - drug effects
Male
Memory - drug effects
Memory Disorders - drug therapy
Memory Disorders - metabolism
Mice
Neuroprotective Agents - chemistry
Neuroprotective Agents - pharmacology
Proto-Oncogene Proteins c-akt - metabolism
Recognition memory
Seeds - chemistry
Signal Transduction - drug effects
title Cassia obtusifolia seed ameliorates amyloid β-induced synaptic dysfunction through anti-inflammatory and Akt/GSK-3β pathways
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