Influence of Carvedilol on Superoxide Generation and Enzyme Release From Stimulated Human Neutrophils

Macicková, T; Pecivová, J; Nosáľ, R; Holománová, D

doi:10.5507/bp.2005.065

Cited by 9 publications

(5 citation statements)

References 20 publications

(6 reference statements)

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“…Glutathione in its reduced form is the most abundant intracellular antioxidant and is involved in the direct scavenging of free radicals or serving as a substrate for the glutathione peroxidase enzyme that catalyzes H 2 O 2 detoxification. Catalase is also known to be a protective enzyme and functions for the detoxification of highly reactive free radicals (Mačičková et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of naringin against cerebellar changes in Alzheimer’s disease through modulation of autophagy, oxidative stress and tau expression: An experimental study

et al. 2022

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Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by gradual cognitive decline. Strong antioxidants that inhibit free radicals, such as polyphenols, reduce the likelihood of developing oxidative stress-related degenerative diseases such as AD. Naringin, a flavonoid found in citrus fruit shown to be neuroprotective, reduce oxidative damage and minimize histopathological changes caused by ischemic reperfusion, enhance the long-term memory in AD animal models. This work aimed to comprehend the role of naringin in the defense of the cerebellum against aluminum chloride (AlCl3)-induced AD in rats by investigating the behavioral, neurochemical, immunohistochemical, and molecular mechanisms that underpin its possible neuroprotective effects. Twenty-four adult albino rats were divided into four groups (n = 6/group): (i) Control (C) received saline per oral (p.o.), (ii) Naringin(N)-received naringin (100 mg/kg/d) p.o, (iii) AlCl3-recived AlCl3 (100 mg/kg/d) p.o and (iv) AlCl3 + Naringin (AlCl3 + N) received both AlCl3 and naringin p.o for 21 days. Behavioral tests showed an increase in the time to reach the platform in Morris water maze, indicating memory impairment in the AlCl3-treated group, but co-administration of naringin showed significant improvement. The Rotarod test demonstrated a decrease in muscle coordination in the AlCl3-treated group, while it was improved in the AlCl3 + N group. Neurochemical analysis of the hippocampus and cerebellum revealed that AlCl3 significantly increased lipid peroxidation and oxidative stress and decreased levels of reduced glutathione. Administration of naringin ameliorated these neurochemical changes via its antioxidant properties. Cerebellar immunohistochemical expression for microtubule assembly (tau protein) and oxidative stress (iNOS) increased in A1C13-treated group. On the other hand, the expression of the autophagic marker (LC3) in the cerebellum showed a marked decline in AlCl3-treated group. Western blot analysis confirmed the cerebellar immunohistochemical findings. Collectively, these findings suggested that naringin could contribute to the combat of oxidative and autophagic stress in the cerebellum of AlCl3-induced AD.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of naringin against cerebellar changes in Alzheimer’s disease through modulation of autophagy, oxidative stress and tau expression: An experimental study

et al. 2022

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“…The oxidative stress is mediated due to free radicals, so it is necessary to account for antioxidant enzymes that serve as the first line of defence against radicals. CAT, GSH, and TBARS enzymes all account for neuron protection in oxidative stress [ 72 ]. GSH levels are known for disrupting neurons in neurodegenerative diseases [ 73 ].…”

Section: Resultsmentioning

confidence: 99%

Effects of Phoenix dactylifera against Streptozotocin‐Aluminium Chloride Induced Alzheimer’s Rats and Their In Silico Study

Ismail

Khalid

Ayub

et al. 2023

BioMed Research International

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Phoenix dactylifera is known for medicinal importance due to its antioxidant, antidiabetic, antidepressant, and anti-inflammatory properties. This study is aimed at evaluating the effect of P. dactylifera seeds to cure Alzheimer’s disease (AD). AD was induced in the rats with streptozotocin + aluminium chloride followed by treatment of methanolic extract of P. dactylifera seeds. The blood glucose levels were determined at regular intervals, which showed a prominent decrease in the extracts treated group. Behavior tests, including the Elevated Plus Maze (EPM) test and Morris Water Maze (MWM) test, were used to evaluate memory patterns in rats. The results indicated that extract-treated rats significantly improved memory behavior compared to the diseased group. After dissection, the serum electrolytes, antioxidant enzymes, and choline esterase enzymes were measured in different organs. The serum parameters creatinine, urea, and bilirubin increased after extract treatment. Similarly, the level of antioxidant enzymes like peroxidases (POD), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and thiobarbituric acid reactive substance (TBARS) in the extract-treated group showed improved results that were close to the normal control group. The enzyme (lipase, insulin, amylase, and acetylcholine) levels were found enhanced in extract groups as compared to diseased rats. High-performance liquid chromatography (HPLC) was used to determine the level of dopamine and serotonin neurotransmitters, which were increased significantly for P. dactylifera seeds with values of 0.18 μg/mg tissue and 0.56 μg/mg tissue, respectively. Overall, results showed that P. dactylifera seeds proved to be quite efficient in improving the memory and behavior of treated rats. The antioxidants and enzymes were also increased; therefore, it may be a potential candidate for treating AD.

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“…Carvedilol has been reported in the literature as acts as a NO modulatory agent in vascular endothelial cells and in cell-free systems (Yoshioka et al, 2000). It has also been shown to inhibit superoxide ion release from activated neutrophils (Maèièkova et al, 2005).Carvedilol also has been shown to preserve the endogenous antioxidant system (i.e., vitamin E andreduced glutathione), which is normally consumedwhen tissues or cells are exposed to oxidative stress . This preservation of endogenous antioxidants may explain why the Carvedilol treatment was able to reverse scopolamine induced cognitive deficit in mice.…”

Section: Discussionmentioning

confidence: 99%

Neuro-protective effect of Carvedilol, an adrenergic antagonist against scopolamine-induced cognitive impairment in mice

Yahaya¹,

Adeola²,

Emma³

2013

J App Pharm Sc

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The use of β-adrenoceptor blocking agents (β -blockers) in the clinical treatment of cardiovascular disorders and glaucoma are associated with enhancedvigilance, attention, reward, learning and memory. The present study was designed to explore the possible role of Carvedilol, an adrenergic antagonist in ameliorating scopolamineinduced neurotoxicity in rats. Mice were divided into control and treatment groups. Control mice for each test received 10 ml normal saline/kg while the treatment groups (n = 6) received Carvedilol (2.5, 5 and 10 mg/kg orally) and1 mg scopolamine/kg intraperitoneally). One hour after sildenafil and thirty minutes after scopolamine administration orally and intraperitoneally respectively, the animals were assessed for 5 minutes on elevated plus maze, Y-maze and open-field. The parametersmeasured on the EPM were memory acquisition and memory retention latencies with and without scopolamine while spontaneous alternation behaviour was measured in Ymaze. The effect of Carvedilol on locomotion was assessed in mice using open field.Carvedilol significantly (p<0.001) shortened memory acquisition and retrieval latencies in mice with scopolamine-induced cognitive deficit. Carvedilol produced significant (p<0.0001) increase in spontaneous alternation behaviour in both memory intact and memory deficit models. Carvedilol however, had no effect on locomotor activity of mice. The results suggest that Carvedilol enhanced memory acquisition and retrieval in cognitive deficit and cognitive intactmice.It also improved short term memory as indicated by increase in spontaneous alternation behaviour in mice.Carvedilol may therefore be useful in management of dementing disorders such as Alzheimer's disease.

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Influence of Carvedilol on Superoxide Generation and Enzyme Release From Stimulated Human Neutrophils

Cited by 9 publications

References 20 publications

Neuroprotective effect of naringin against cerebellar changes in Alzheimer’s disease through modulation of autophagy, oxidative stress and tau expression: An experimental study

Neuroprotective effect of naringin against cerebellar changes in Alzheimer’s disease through modulation of autophagy, oxidative stress and tau expression: An experimental study

Effects of Phoenix dactylifera against Streptozotocin‐Aluminium Chloride Induced Alzheimer’s Rats and Their In Silico Study

Neuro-protective effect of Carvedilol, an adrenergic antagonist against scopolamine-induced cognitive impairment in mice

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