Features of the extrapancreatic action of glibenclamide in cerebral ischemia in the highlands

The features of remodeling of the components of the vascular plexus and the microcirculatory bed of the brain in cerebral ischemia in the highlands are studied, the features of the action of glibenclamide on these structures are presented. It is shown that the sulfonylurea receptor 1 (SUR 1) in the highlands becomes more sensitive to glibenclamide than in the low mountains. Key words: brain, ischemia, glibenclamide, highlands.

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Neuroprotective and cerebrovascular effects of endogenous N-Arachidonoyl-GABA and its putative Cox-2 metabolite – GABA conjugate with Prostaglandin E2

Research Results in Pharmacology ◽

10.3897/rrpharmacology.7.70974 ◽

2021 ◽

Vol 7 (3) ◽

pp. 49-61

Author(s):

Narine R. Mirzoyan ◽

Nelly G. Khostikyan ◽

Vahe S. Meliksetyan ◽

Arpine A. Hakobyan ◽

Tamara S. Gan’shina ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Ischemia ◽

Prostaglandin E2 ◽

Brain Tissue ◽

Brain Ischemia ◽

Cerebral Circulation ◽

Transient Ischemia ◽

Cox 2 ◽

The Brain ◽

Rat Brain Tissue

Introduction: The aim of the study was to compare the neuroprotective and cerebrovascular effects of bioactive, endogenous lipid – N-arachidonoyl-GABA (AA-GABA) and GABA conjugate with prostaglandin E2 (PGE2-GABA) by evaluation of a morphological state of rat brain tissue and lipofuscin levels under the condition of permanent focal brain ischemia, as well as cerebral circulation under the condition of global transient ischemia. Materials and methods: The study has been implemented using the models of the left middle cerebral artery occlusion (MCAO) and global transient ischemia of the brain. A morphological examination of the brain tissue, a registration of local blood flow by laser flowmeter, and quantitative measurement of lipofuscin by fluorescence spectroscopy were used. Results and discussion: AA-GABA and the putative COX-2 metabolite PGE2-GABA showed significant neuroprotective and cerebrovascular effects in rat models of global and focal cerebral ischemia. In the MCAO model, AA-GABA and PGE2-GABA at a dose of 2 mg/kg/day administered i.p. for 6 or 12 days led to: 1) significant restoration of neurons and glial cells with intracellular regeneration of cytoplasmic and nuclear structures, 2) decrease in brain tissue edema; 3) attenuated thrombosis and stasis, and 4) absence of large necrotic foci in rat brain tissue. AA-GABA and PGE2-GABA at the same dose prevented excessive accumulation of lipofuscin in both brain hemispheres in rats with MCAO. All the studied compounds increase cerebral blood circulation in rats subjected to global transient ischemia. However, the cerebrovascular effect of PGE2-GABA was superior to the activity of AA-GABA and all other tested compounds. AA-GABA and PGE2-GABA, unlike PGE2 and nimodipine, increase the cerebral blood flow in rats with global transient brain ischemia and have no influence on the intact animals. Apparently, the GABAergic vascular system of the brain is involved in the mechanisms of the neuroprotective action of AA-GABA and PGE2-GABA. Conclusion: For the first time, we demonstrated the ability of AA-GABA and its putative metabolite COX-2 PGE2-GABA to improve cerebral circulation, attenuate structural damage and lipofuscin accumulation during cerebral ischemia. The natural origin of AA-GABA, which possesses neuroprotective and cerebrovascular activity, as well as anti-aggregatory activity, allows considering AA-GABA as one of the endogenous protective factors in ischemic brain lesions. Graphical abstract:

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Chronic Brain Ischemia: From Risk Factors to Cerebrovascular Complications

Bulletin of Science and Practice ◽

10.33619/2414-2948/67/30 ◽

2021 ◽

Vol 7 (6) ◽

Author(s):

F. Yusupov ◽

Sh. Nurmatov ◽

N. Abdykalykova ◽

A. Yuldashev ◽

M. Abdykadyrov

Keyword(s):

Risk Factors ◽

Cerebral Ischemia ◽

Arterial Hypertension ◽

Brain Tissue ◽

Brain Ischemia ◽

Chronic Cerebral Ischemia ◽

Cerebrovascular Complications ◽

Cerebral Blood Supply ◽

Chronic Brain Ischemia ◽

The Brain

Chronic cerebral ischemia is a polyetiological, chronic progressive dysfunction of the brain caused by diffuse and / or small focal damage to the brain tissue in conditions of prolonged insufficiency of cerebral blood supply. The review reflects the current understanding of chronic cerebral ischemia. The main pathogenetic mechanisms of the onset of chronic cerebral ischemia in patients with arterial hypertension, atherosclerosis and smoking are outlined.

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Neuroprotection and Angiogenesis: Dual Role of Erythropoietin in Brain Ischemia

Physiology ◽

10.1152/physiologyonline.2000.15.5.225 ◽

2000 ◽

Vol 15 (5) ◽

pp. 225-229 ◽

Cited By ~ 11

Author(s):

Hugo H. Marti ◽

Myriam Bernaudin ◽

Edwige Petit ◽

Christian Bauer

Keyword(s):

Cerebral Ischemia ◽

Growth Factor ◽

Protective Effect ◽

Brain Tissue ◽

Brain Ischemia ◽

Vessel Growth ◽

The Brain ◽

Indirect Protection ◽

Brain Vessel

Erythropoietin, originally defined as an erythroid growth factor, is upregulated in the brain under conditions of hypoxia. So far, two functions have been identified for this locally produced cytokine: a direct protective effect on neuronal cells during cerebral ischemia and an indirect protection of brain tissue that could be provided by promoting brain vessel growth.

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ГЕНДЕРНЫЕ РАЗЛИЧИЯ КОГНИТИВНЫХ ФУНКЦИЙ ПРИ ЦЕРЕБРОВАСКУЛЯРНОЙ ПАТОЛОГИИ

World Science ◽

10.31435/rsglobal_ws/31102018/6176 ◽

2018 ◽

Vol 1 (10(38)) ◽

pp. 33-36

Author(s):

Аликулова Н. А. ◽

Назарова Ж. А. ◽

Рахматова С. Н.

Keyword(s):

Cognitive Impairment ◽

Cerebral Ischemia ◽

Evoked Potentials ◽

Brain Ischemia ◽

Hypertensive Disease ◽

Neuropsychological Examination ◽

Cognitive Evoked Potentials ◽

Chronic Brain Ischemia ◽

The Brain ◽

Low Rate

Clinical, instrumental and neuropsychological examination was carried out in 110 patients with chronic brain ischemia of the 2nd degree on the background of hypertension of the 2nd stage. The subjects were divided into 2 groups based on gender. Signs of venous cerebral dishelie valley significantly more cases in the group of women. It is shown that the group of women with cerebral venous Disgaea more patients had cognitive impairment (MMSE scale). Also, the low rate of induced cognitive potentials in the brain (the method of cognitive evoked potentials) was more pronounced in women than in men. It should be assumed that in hypertensive disease, the presence of concomitant cerebral venous dysfunction aggravates the course of cerebral ischemia, especially in women.

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

Journal of Clinical and Medical Research ◽

10.37191/mapsci-2582-4333-2(5)-045 ◽

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.

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DNA Damage and Repair in the Brain After Cerebral Ischemia

Current Topics in Medicinal Chemistry ◽

10.2174/1568026013394688 ◽

2001 ◽

Vol 1 (6) ◽

pp. 483-495 ◽

Cited By ~ 13

Author(s):

Bentham Science Publisher Philip K. Liu

Keyword(s):

Dna Damage ◽

Cerebral Ischemia ◽

Dna Damage And Repair ◽

The Brain

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

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527319999200831153748 ◽

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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Effects of Buyang Huanwu Tang Combined with Bone Marrow Mesenchymal Stem Cell Transplantation on the Expression of VEGF and Ki-67 in the Brain Tissue of the Cerebral Ischemia-Reperfusion Model Rat

Journal of Traditional Chinese Medicine ◽

10.1016/s0254-6272(10)60056-8 ◽

2010 ◽

Vol 30 (4) ◽

pp. 278-282 ◽

Cited By ~ 19

Author(s):

Yun-ke ZHANG ◽

Xue-yong HAN ◽

Zhi-ying CHE

Keyword(s):

Bone Marrow ◽

Stem Cell ◽

Cerebral Ischemia ◽

Mesenchymal Stem Cell ◽

Stem Cell Transplantation ◽

Ischemia Reperfusion ◽

Ki 67 ◽

Mesenchymal Stem Cell Transplantation ◽

Cerebral Ischemia Reperfusion ◽

The Brain

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Zingiber officinaleMitigates Brain Damage and Improves Memory Impairment in Focal Cerebral Ischemic Rat

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2011/429505 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 35

Author(s):

Jintanaporn Wattanathorn ◽

Jinatta Jittiwat ◽

Terdthai Tongun ◽

Supaporn Muchimapura ◽

Kornkanok Ingkaninan

Keyword(s):

Cognitive Function ◽

Cerebral Ischemia ◽

Brain Damage ◽

Focal Cerebral Ischemia ◽

Infarct Volume ◽

Neuroprotective Effect ◽

Morris Water Maze Test ◽

Brain Infarct ◽

Ginger Rhizome ◽

The Brain

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.

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