Pharmacological modulation of I1-imidazoline and α2-adrenoceptors in sub acute brain ischemia induced vascular dementia

Gupta, Surbhi; Sharma, Bhupesh

doi:10.1016/j.ejphar.2013.12.003

Cited by 31 publications

(15 citation statements)

References 94 publications

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“…The moxonidine-evoked MDA suppression (Fig. 8B, C) agrees with reported findings following brain ischemia (Gupta and Sharma, 2014). Finally, pharmacologic inhibition of CSE activity, which abrogated moxonidine ability to restore H 2 S (Fig.…”

Section: Discussionsupporting

confidence: 91%

Cystathionine-γ lyase-derived hydrogen sulfide mediates the cardiovascular protective effects of moxonidine in diabetic rats

El-Sayed

Zakaria

Abdel-Ghany

et al. 2016

European Journal of Pharmacology

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Blunted cystathionine-γ lyase (CSE) activity (reduced endogenous H2S-level) is implicated in hypertension and myocardial dysfunction in diabetes. Here, we tested the hypothesis that CSE derived H2S mediates the cardiovascular protection conferred by the imidazoline I1 receptor agonist moxonidine in a diabetic rat model. We utilized streptozotocin (STZ; 55 mg/kg i.p) to induce diabetes in male Wistar rats. Four weeks later, STZ-treated rats received vehicle, moxonidine (2 or 6 mg/kg; gavage), CSE inhibitor DL-propargylglycine, (37.5 mg/kg i.p) or DL-propargylglycine with moxonidine (6 mg/kg) for 3 weeks. Moxonidine improved the glycemic state, and reversed myocardial hypertrophy, hypertension and baroreflex dysfunction in STZ-treated rats. Ex vivo studies revealed that STZ caused reductions in CSE expression/activity, H2S and nitric oxide (NO) levels and serum adiponectin and elevations in myocardial imidazoline I1 receptor expression, p38 and extracellular signal-regulated kinase, ERK1/2, phosphorylation and lipid peroxidation (expressed as malondialdehyde). Moxonidine reversed these biochemical responses, and suppressed the expression of death associated protein kinase-3. Finally, pharmacologic CSE inhibition (DL-propargylglycine) abrogated the favorable cardiovascular, glycemic and biochemical responses elicited by moxonidine. These findings present the first evidence for a mechanistic role for CSE derived H2S in the glycemic control and in the favorable cardiovascular effects conferred by imidazoline I1 receptor activation (moxonidine) in a diabetic rat model.

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Section: Discussionsupporting

confidence: 91%

Cystathionine-γ lyase-derived hydrogen sulfide mediates the cardiovascular protective effects of moxonidine in diabetic rats

El-Sayed

Zakaria

Abdel-Ghany

et al. 2016

European Journal of Pharmacology

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“…Vascular dementia is usually characterized by cognitive impairments, such as deficits in attention and executive function . A persistent shortage in cerebral blood flow leads to ischaemia of the brain tissue and reduced levels of oxygen and nutrients, resulting in cell death . Oxidative stress is postulated to play a critical role in vascular dementia .…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of zafirlukast, piracetam and their combination on L‐Methionine‐induced vascular dementia in rats

Fayez

Elnoby

Bahnasawy

et al. 2019

Fundamemntal Clinical Pharma

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Vascular dementia is considered a vascular cognitive impairment disease caused by neuronal degeneration in the brain. Several studies have supported the hypothesis that oxidative stress and endothelial dysfunction are the main pathogenic factors in vascular dementia. This current study aims to determine the possible neuroprotective effects of zafirlukast, piracetam and the combination of piracetam and zafirlukast on L‐methionine‐induced vascular dementia in rats. Male Wistar albino rats were divided into five groups. Group I was the normal control, and group II received L‐methionine (1700 mg/kg, P.O.) for 32 days. The remaining groups received zafirlukast (20 mg/kg, P.O.), piracetam (600 mg/kg, P.O.) or their combination (zafirlukast 20 mg/kg + piracetam 600 mg/kg, P.O.) for 32 days after L‐methionine administration. Afterwards, the cognitive and memory performances of the rats were investigated using the novel object recognition (NOR) test; rats were then sacrificed for histopathological and biochemical analyses. L‐methionine‐induced vascular dementia altered rats’ behaviours and the brain contents of different neurotransmitters and acetylcholinesterase activity while increasing levels of oxidative stress and causing notable histopathological alterations in brain tissues. The treatment of vascular dementia with zafirlukast and the combination improved neurochemical, behavioural and histological alterations to a comparable level to those of piracetam. Thus, zafirlukast, piracetam and the combination of both drugs can be considered as potential therapeutic strategies for the treatment of vascular dementia induced by L‐methionine. To the best of our knowledge, this study is the first to explore the neuroprotective effects of zafirlukast and piracetam on L‐methionine‐induced vascular dementia.

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“…DA can regulate voluntary movement, which plays an important role in improving memory (Wan et al, 2014;Saddoris et al, 2015), while 5-HT, synthesized in the brain nerve cells and important to maintain normal intelligence, whose role is to keep the synaptic connection of cortex and hippocampus and involve in the brain's cognitive function. When VD occurs, DA and 5-HT systems damage, so the deficiency in DA and 5-HT synthesis can lead to cognitive dysfunction and behavioral disorder of patient with dementia (Gupta and Sharma, 2014). In this study, DA and 5-HT levels in brain cortical tissue of VD model rats were detected, and the results showed that their levels in model group were significantly decreased.…”

Section: Comparison Of Da and 5-th Levels Of Rats In Each Groupmentioning

confidence: 60%

Effect of Ginkgo biloba extract on cognitive function and neurotransmitter levels in rats with vascular dementia

Wang

Shan

Wang

et al. 2017

IJAR

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This study aimed to investigate the effect of Ginkgo biloba extract on the cognitive function and neurotransmitter levels in rats with vascular dementia (VD) and its mechanism of action. 50 male Sprague Dawley rats were selected for this study, and the vascular dementia model was established by permanent occlusion of bilateral common carotid arteries of rats. Of which 40 rats were then divided into four groups (n=10): vascular dementia group, low-dose, middle-dose and high-dose ginkgo biloba extract groups respectively; another 10 rats were allocated to sham operation group. Rats in low, middle and high dose groups were received 5, 10 and 20 mg/kg/d Ginkgo biloba extract via tail vein, respectively, while model group and sham group received an equal volume of normal saline. Morris water maze was used to evaluate the cognitive function of rats. After behavioral observation, these rats were sacrificed for detecting the level of acetylcholine (ACh), dopamine (DA) and 5-hydroxytryptamine (5-HT) in brain tissue. Ginkgo biloba extract can significantly improve the cognitive function of rats with vascular dementia, the mechanism may be correlated with the fact that the extract can obviously increase the levels of ACh, 5-HT and DA, as well as inhibit the activity of AChE.

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Pharmacological modulation of I1-imidazoline and α2-adrenoceptors in sub acute brain ischemia induced vascular dementia

Cited by 31 publications

References 94 publications

Cystathionine-γ lyase-derived hydrogen sulfide mediates the cardiovascular protective effects of moxonidine in diabetic rats

Cystathionine-γ lyase-derived hydrogen sulfide mediates the cardiovascular protective effects of moxonidine in diabetic rats

Neuroprotective effects of zafirlukast, piracetam and their combination on L‐Methionine‐induced vascular dementia in rats

Effect of Ginkgo biloba extract on cognitive function and neurotransmitter levels in rats with vascular dementia

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