Bombesin attenuated ischemia-induced spatial cognitive and synaptic plasticity impairment associated with oxidative damage

Yao, Yang; Wang, Faqi; Yang, Xiaozhong; Zang, Dawei; Yang, Jiajia; Wang, Zhiyun

doi:10.1016/j.biopha.2018.03.155

Cited by 7 publications

(8 citation statements)

References 42 publications

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“…Synaptic transmission and plasticity are the basis of learning and memory; thus, this present study examined whether or not the embelin administration can affect the long-term potentiation (LTP) in hippocampal of BCCAO model. Based on results, synaptic plasticity was found significantly impaired in BCCAO rats, which was in agreement with those of previous studies 12,24,25 . Interestingly, the adverse effect of chronic cerebral hypoperfusion on LTP was significantly attenuated after treatment with 0.3 mg/kg embelin.…”

Section: Discussionsupporting

confidence: 93%

“…37 from the observation of a significant decrease in SOD1 mRNA expression level of the BCCAO rats’ hippocampus. Interestingly, administrating embelin has significantly increased the SOD1 mRNA expression level, which indicates the antioxidant action of embelin that might be attributed to a direct receptor-mediated mechanism activating the downstream protein kinase signalling pathways and intracellular antioxidant enzyme systems 25 .…”

Section: Discussionmentioning

confidence: 95%

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Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion

Bhuvanendran

Bakar

Kumari

et al. 2019

Sci Rep

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Alzheimer’s disease (AD) is the second most occurring neurological disorder after stroke and is associated with cerebral hypoperfusion, possibly contributing to cognitive impairment. In the present study, neuroprotective and anti-AD effects of embelin were evaluated in chronic cerebral hypoperfusion (CCH) rat model using permanent bilateral common carotid artery occlusion (BCCAO) method. Rats were administered with embelin at doses of 0.3, 0.6 or 1.2 mg/kg (i.p) on day 14 post-surgery and tested in Morris water maze (MWM) followed by electrophysiological recordings to access cognitive abilities and synaptic plasticity. The hippocampal brain regions were extracted for gene expression and neurotransmitters analysis. Treatment with embelin at the doses of 0.3 and 0.6 mg/kg significantly reversed the spatial memory impairment induced by CCH in rats. Embelin treatment has significantly protected synaptic plasticity impairment as assessed by hippocampal long-term potentiation (LTP) test. The mechanism of this study demonstrated that embelin treatment alleviated the decreased expression of BDNF, CREB1, APP, Mapt, SOD1 and NFκB mRNA levels caused by CCH rats. Furthermore, treatment with embelin demonstrated neuromodulatory activity by its ability to restore hippocampal neurotransmitters. Overall these data suggest that embelin improve memory and synaptic plasticity impairment in CCH rats and can be a potential drug candidate for neurodegenerative disease-related cognitive disorders.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion

Bhuvanendran

Bakar

Kumari

et al. 2019

Sci Rep

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“…20 Yao et al found that bombesin significantly increased the reduction of total superoxide dismutase and catalase activities and decreased malondialdehyde content in cognitively impaired rats, suggesting that GRPR (which can also bind with bombesin in rodents) could attenuate cerebral ischemiainduced memory deficits and synaptic damage by inhibiting oxidative stress. 21 2.2. Fear (Amygdala).…”

Section: Memory and Cognition (Hippocampus)mentioning

confidence: 99%

“…11,12,14,16,20,21 Fear Amygdala Enhancing inhibitory effects on principal neurons, negatively modulating LTP in LA and long-term fear memory. Knocking out GRPR decreases the basal firing rate of CeM neurons and modifies short-term but not long-term synaptic plasticity in LA.…”

mentioning

confidence: 99%

Role of the GRP/GRPR System in Regulating Brain Functions

Zhao,

Chen,

Dai

et al. 2023

ACS Chem. Neurosci.

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“…With the onset of progressive neurodegenerative disorder, VD should be focused on the early stage of pathological process, especially synaptic dysfunction. Increasing evidence has shown that lack of synaptic associated proteins (Carlson et al, 2017 ; Casaletto et al, 2017 ; Li et al, 2017a , b ; Liu et al, 2017 ; Yao et al, 2018 ) contributes to synaptic dysfunction, and even slight perturbations of synapse function can lead to brain disorders (van den Maagdenberg and Plomp, 2003 ; Cesca et al, 2010 ). The mechanism of chronic ischemia-induced cognitive impairment has been studied extensively (Choi et al, 2015 ; Wan et al, 2017 ; Wang et al, 2017 , 2018b ; Yao et al, 2018 ), whereas the mechanism of synapse dysfunction in the early stage of VD remains unclear.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-210-5p Contributes to Cognitive Impairment in Early Vascular Dementia Rat Model Through Targeting Snap25

Ren

et al. 2018

Front. Mol. Neurosci.

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Vascular dementia (VD) is the most common form of dementia in elderly people. However, little is understood about the role of microRNAs (miRNAs) involved in cognitive impairment in early VD. Here, a VD model induced by chronic cerebral ischemia and fetal bovine serum (FBS)-free cell model that detects synapse formation was established to investigate the function of miRNAs in early VD. The microarray analysis and real-time reverse transcription polymerase chain reaction (RT-PCR) showed that miR-210-5p increased significantly in the hippocampus of rats with 4 weeks of ischemia. The VD model rats also displayed significant cognitive deficits and synaptic loss. The overexpression of miR-210-5p decreased the synaptic number in primary hippocampal neurons, whereas specific suppression of miR-210-5p resulted in the formation of more synapses. Additionally, intracerebroventricular (ICV) injection of miR-210-5p agomir to VD rats aggravated phenotypes of cognitive impairment and synaptic loss. These VD-induced phenotypes were effectively attenuated by miR-210-5p antagomir. Moreover, bioinformatic prediction revealed that synaptosomal-associated protein of 25 KDa (Snap25) mRNA is targeted by miR-210-5p. The miR-210-5p decreased the luciferase activities of 3’ untranslated region (3’UTR) of Snap25 mRNA. Mutation of predicted miR-210-5p binding sites in the 3’ UTR of Snap25 mRNA abolished the miR-210-5p-induced decrease in luciferase activity. Western blot and immunofluorescence staining confirmed that miR-210-5p targets Snap25. Finally, RT-quantitative PCR (qPCR) and immunofluorescence staining detected that miR-210-5p agomir downregulated Snap25 expression in the cornu ammonis1 (CA1) region of hippocampi in VD rats, whereas miR-210-5p antagomir upregulated Snap25 expression. Altogether, miR-210-5p contributes to cognitive impairment in chronic ischemia-induced VD model through the regulation of Snap25 expression, which potentially provides an opportunity to develop a new therapeutic strategy for VD.

show abstract

Bombesin attenuated ischemia-induced spatial cognitive and synaptic plasticity impairment associated with oxidative damage

Cited by 7 publications

References 42 publications

Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion

Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion

Role of the GRP/GRPR System in Regulating Brain Functions

MicroRNA-210-5p Contributes to Cognitive Impairment in Early Vascular Dementia Rat Model Through Targeting Snap25

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