Expression of HSP70 in the brain of rats during experimental cerebral ischemia modeling and on the background of neuroprotection

2017 ◽  
Vol 4 ◽  
pp. 105-111
Author(s):  
I.F. Belenichev ◽  
S.V. Pavlov ◽  
N.V. Bukhtiayarova ◽  
I.B. Samura ◽  
A.N. Egorov ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
The Brain ◽  
Experimental Cerebral Ischemia

scholarly journals METHODS FOR ESTIMATING NEUROLOGICAL DISTURBANCES IN EXPERIMENTAL CEREBRAL ISCHEMIA

Biomeditsina ◽  
2019 ◽  
pp. 69-74
Author(s):  
E. I. Bon ◽  
N. Ye. Maksimovich
Keyword(s):  
Cerebral Ischemia ◽  
Muscle Strength ◽  
Neurological Deficit ◽  
Laboratory Animals ◽  
Control Group ◽  
Brain Pathology ◽  
Behavioural Disorders ◽  
Resistance To Hypoxia ◽  
The Brain ◽  
Experimental Cerebral Ischemia

Investigation of the brain pathology in experimental ischemia requires adequate methods for assessing the neurological deficit that occurs in laboratory animals, including sensory-based and behavioural disorders. In this research, we aimed to compare motor and behavioural disorders in rats with partial and subtotal experimental cerebral ischemia. The rats modelled with cerebral ischemia are found to exhibit a decrease in muscle strength, resistance to hypoxia, motor and emotional activity. The animals with incomplete cerebral ischemia demonstrated more pronounced sensory-based motor and behavioural disorders compared both with those modelled with partial cerebral ischemia and, in particular, with the control group.

scholarly journals The effects of hyper-, normo- and hypoglycemia on pathological changes of the brain in experimental cerebral ischemia

Nosotchu ◽  
1984 ◽  
Vol 6 (4) ◽  
pp. 487-494
Author(s):  
Setsuro Ibayashi ◽  
Jun Ogata ◽  
Masatoshi Fujishima ◽  
Seizo Sadoshima ◽  
Teruo Omae
Keyword(s):  
Cerebral Ischemia ◽  
Pathological Changes ◽  
The Brain ◽  
Experimental Cerebral Ischemia

Exploring the Role of Remote Ischemic Preconditioning In Long Term Cognitive Impairment after Global Ischemia-Reperfusion-Induced Vascular Dementia in Mice

2020 ◽  
Author(s):  
Amteshwar Singh Jaggi
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Ischemia ◽  
Vascular Dementia ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Cerebral Ischemic ◽  
The Brain

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

DNA Damage and Repair in the Brain After Cerebral Ischemia

2001 ◽  
Vol 1 (6) ◽  
pp. 483-495 ◽  
Author(s):  
Bentham Science Publisher Philip K. Liu
Keyword(s):  
Dna Damage ◽  
Cerebral Ischemia ◽  
Dna Damage And Repair ◽  
The Brain

Minocycline inhibits mTOR signaling activation and alleviates behavioral deficits in the Wistar rats with acute ischemia stroke

2020 ◽  
Vol 19 ◽  
Author(s):  
Shengyuan Wang ◽  
Chuanling Wang ◽  
Lihua Wang ◽  
Zhiyou Cai
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Acute Ischemia ◽  
Intragastric Administration ◽  
Underlying Mechanisms ◽  
Signaling Activation ◽  
The Brain ◽  
Minocycline Therapy

Background: Mammalian target of rapamycin (mTOR) has been evidenced as a multimodal therapy in the path-ophysiological process of acute ischemic stroke (AIS). However, the pathway that minocycline targets mTOR signaling is not fully defined in the AIS pathogenesis. This study is to aim at the effects of minocycline on the mTOR signaling in the AIS process and further discover the underlying mechanisms of minocycline involved in the following change of mTOR signaling-autophagy. Methods: Cerebral ischemia/reperfusion (CIR) rat animal models were established with the transient suture occlusion into middle cerebral artery. Minocycline (50mg/kg) was given by intragastric administration. The Morris water maze was used to test the cognitive function of animals. Immunohistochemistry and immunofluorescence were introduced for testing the lev-els of synaptophysin and PSD-95. Western blot was conducted for investigating the levels of mTOR, p-mTOR (Ser2448), p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366), p-eIF4B (Ser406), LC3, p62, synaptophysin and PSD-95. Results: Minocycline prevents cognitive decline of the MCAO stroke rats. Minocycline limits the expression of p-mTOR (Ser2448) and the downstream targets of mTOR [p70S6, p-p70S6 (Thr389), eEF2k, p-eEF2k (Ser366) and p-eIF4B (Ser406)] (P<0.01), while minocycline has no influence on mTOR. LC3-II abundance and the LC3-II/I ratio were upregu-lated in the hippocampus of the MCAO stroke rats by the minocycline therapy (P<0.01). p62 was downregulated in the hippocampus from the MCAO stroke rats administrated with minocycline therapy(P<0.01). The levels of SYP and PSD-95 were up-regulated in the brain of the MCAO stroke rats administrated with minocycline therapy. Conclusion: Minocycline prevents cognitive deficits via inhibiting mTOR signaling and enhancing autophagy process, and promoting the expression of pre-and postsynaptic proteins (synaptophysin and PSD-95) in the brain of the MCAO stroke rats. The potential neuroprotective role of minocycline in the process of cerebral ischemia may be related to mitigating is-chemia-induced synapse injury via inhibiting activation of mTOR signaling.

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