Carvacrol suppresses learning and memory dysfunction and hippocampal damages caused by chronic cerebral hypoperfusion

2019 ◽  
Vol 393 (4) ◽  
pp. 581-589 ◽  
Author(s):  
Azadeh Shahrokhi Raeini ◽  
Zeynab Hafizibarjin ◽  
Mohammad Ebrahim Rezvani ◽  
Fatemeh Safari ◽  
Faezeh Afkhami Aghda ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zhao-Hui Yao ◽  
Xiao-li Yao ◽  
Shao-feng Zhang ◽  
Ji-chang Hu ◽  
Yong Zhang

Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.


Molecules ◽  
2015 ◽  
Vol 20 (2) ◽  
pp. 1904-1921 ◽  
Author(s):  
Sooyong Kim ◽  
Il-Hwan Kang ◽  
Jung-Bum Nam ◽  
Yoonchul Cho ◽  
Doo-Young Chung ◽  
...  

2021 ◽  
Vol 4 (2) ◽  
pp. 1-13
Author(s):  
Kesevan Rajah Kumaran ◽  
Habibah Abdul Wahab ◽  
Zurina Hassan

Vascular dementia (VaD), is one of the most common types of dementia in the ageing population, initiated by chronic cerebral hypoperfusion (CCH). At present, effective therapeutic approaches to cure VaD are still missing. Cholinergic system dysfunction in the central nervous system (CNS) has been recognised as one of the main reasons for learning and memory impairment in VaD patients. Therefore, medications that restore the level of acetylcholine (ACh) neurotransmitter by inhibiting cholinesterase activity were proposed as a potential candidate to treat VaD patients. Permanent occlusion of bilateral common carotid arteries (POBCCA) surgery method was performed to develop CCH model in rats. The present study evaluated the anti-cholinesterase activity of three Malaysian plant methanol leaf extracts in vitro and further validated its cognitive-enhancing effects in vivo using POBCCA rats. The selected plant extracts were Coccoloba uvifera (stems), Mimusops elengi (leaves) and Syzygium aqueum (leaves). The in vitro anti-cholinesterase activities of these plants were determined using Ellman's method. The effects of selected plant extracts (100 and 200 mg/kg, p.o.) on learning and memory functions were evaluated using a series of behavioural tests. All the selected plant extracts exhibited good anti-acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities in vitro, with IC50 ranging from 3.67 to 16.04 and 5.6 to 13.95 µg/mL, respectively. Extracts of S. aqueum (200 mg/kg) improve both short- and long-term recognition memories, whereas M. elengi and S. aqueum (200 mg/kg) extracts improve spatial learning. None of the extracts impaired motor and exploratory functions in POBCCA rats. In conclusion, methanol extracts of C. uvifera, M. elengi and S. aqueum showed good anti-cholinesterase activity in vitro. However, only M. elengi and S. aqueum improve learning and memory function in POBCCA rats.


2015 ◽  
Vol 1120-1121 ◽  
pp. 853-856
Author(s):  
Li Tang ◽  
Yu Li

Vascular dementia (VD) is the cognitive impairment clinical syndrome caused by various cerebrovascular diseases. At present the exact causes of VD are not clear, it is believed that ischemic cerebral vascular disease is one of the factors. Hypertension, hyperlipidemia, diabetes, tobacco and alcohol addiction are risk factors of VD. Most of them can be traced back to the youth. Curcumin has a neuroprotective effect in Alzheimer’s disease (AD) and other neurodegenerative diseases. But the effect of curcumin on brain injury caused by chronic cerebral hypoperfusion was unclear. In this study, chronic cerebral ischemia model was used to investigate the effect of curcumin on learning and memory ability of young and aged rats and to explore the mechanism of neuroprotective effect of Curcumin. The result showed that Curcumin can reduce the brain damage both in young and aged VD rats and improve learning and memory ability, and the effect was dose-dependent, without age difference. The pathological injury of the hippocampus might be one of the mechanisms of curcumin improving cognitive impairment of VD rats.


Oncotarget ◽  
2017 ◽  
Vol 8 (64) ◽  
pp. 107920-107931 ◽  
Author(s):  
Na Wei ◽  
Kai Zheng ◽  
Rui Xue ◽  
Sheng-Li Ma ◽  
Hua-Yan Ren ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document