Neuroprotective role of naringenin on carbaryl induced neurotoxicity in mouse neuroblastoma cells

Muthaiah, Vijaya Prakash Krishnan; Venkitasamy, Lavanya; Prakash, Seppan; Chandrasekar, Kirubhanand; Venkatachalam, Sankar

doi:10.4103/0976-500x.114599

Cited by 35 publications

(8 citation statements)

References 19 publications

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“…In addition, naringenin improved survival of mouse neuroblastoma cells following carbaryl-induced toxicity, reduced oxidative stress (by mitigating ROS), and suppressed apoptosis (by inhibiting Bax, caspase-3 and upregulating Bcl-2). It also restored a depletion of mitochondrial membrane potential induced by carbaryl [138].…”

Section: Naringenin In Neurodegenerative Diseasesmentioning

confidence: 99%

On the Neuroprotective Effects of Naringenin: Pharmacological Targets, Signaling Pathways, Molecular Mechanisms, and Clinical Perspective

et al. 2019

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As a group of progressive, chronic, and disabling disorders, neurodegenerative diseases (NDs) affect millions of people worldwide, and are on the rise. NDs are known as the gradual loss of neurons; however, their pathophysiological mechanisms have not been precisely revealed. Due to the complex pathophysiological mechanisms behind the neurodegeneration, investigating effective and multi-target treatments has remained a clinical challenge. Besides, appropriate neuroprotective agents are still lacking, which raises the need for new therapeutic agents. In recent years, several reports have introduced naturally-derived compounds as promising alternative treatments for NDs. Among natural entities, flavonoids are multi-target alternatives affecting different pathogenesis mechanisms in neurodegeneration. Naringenin is a natural flavonoid possessing neuroprotective activities. Increasing evidence has attained special attention on the variety of therapeutic targets along with complex signaling pathways for naringenin, which suggest its possible therapeutic applications in several NDs. Here, in this review, the neuroprotective effects of naringenin, as well as its related pharmacological targets, signaling pathways, molecular mechanisms, and clinical perspective, are described. Moreover, the need to develop novel naringenin delivery systems is also discussed to solve its widespread pharmacokinetic limitation.

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Section: Naringenin In Neurodegenerative Diseasesmentioning

confidence: 99%

On the Neuroprotective Effects of Naringenin: Pharmacological Targets, Signaling Pathways, Molecular Mechanisms, and Clinical Perspective

et al. 2019

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“…[ 17 ] Also, naringenin supplementation has shown to restore expression of choline acetyl transferase and improvement in learning and memory. [ 16 18 ] Cytokine regulation and inflammation control by naringenin in brain via TNF-α and IL-1β have also been reported. [ 19 ]…”

Section: Introductionmentioning

confidence: 99%

Effect of naringenin (A naturally occurring flavanone) against pilocarpine-induced status epilepticus and oxidative stress in mice

Shakeel¹,

Rehman

Tabassum³

et al. 2017

Phcog Mag

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Background:Epilepsy is a disorder of the central nervous system characterized by recurrent seizures. It is a very common disease in which approximately 30% of patients do not respond favourably to treatment with anticonvulsants. Oxidative stress is associated with neuronal damage arising from epileptic seizures. The present study investigated the effects of naringenin in pilocarpine-induced epilepsy in mice. Naringenin, one of the most frequently occurring flavanone in citrus fruits, was evaluated for its shielding effect against the pilocarpine induced behavioural, oxidative and histopathological alterations in rodent model of epilepsy.Methodology:Epilepsy was induced by giving pilocarpine (300mg/kg) and sodium valproate (300mg/kg) was given as standard anti-epileptic drug Pilocarpine was administered (300 mg /kg body weight) intraperitoneally to the mice on 15th day while naringenin was administered orally (20 and 40 mg/kg body weight) for 15 days prior to administration of pilocarpine.Results:The intraperitoneal administration of pilocarpine enhanced lipid peroxidation, caused reduction in antioxidant enzymes, viz., catalase, superoxide dismutase and glutathione reductase. Treatment of mice orally with naringenin (20 mg/kg body weight and 40 mg/kg body weight) resulted in a significant decrease in lipid peroxidation. There was significant recovery of glutathione content and all the antioxidant enzymes studied. Also in case of behavioural parameters studied, naringenin showed decrease in seizure severity. All these changes were supported by histological observations, which revealed excellent improvement in neuronal damage.Conclusion:The higher dose of naringenin was more potent in our study and was comparable to the standard drug (sodium valproate) in effectiveness.SUMMARY Naringenin ameliorated the development of ROS formation in hippocamus.Naringenin helped in recovery of antioxidant enzymes.Naringenin decreased seizure severity.Naringenin treatment reduced lipid peroxidation. Abbreviations used: 6-OHDA: 6-hydroxydopamine, AED: Anti epileptic drugs, AIDS: Acquired immune deficiency syndrome, ANOVA: Analysis of variance, ATP: Adenosine triphosphate, CA: Cornu ammonis, CAT: Catalase, DG: Dentate gyrus, EDTA: Ethylenediamine tetra acetic acid, GR: Glutathione reductase, GSH: Glutathione reduced, HCl: Hydrochloric acid, IL-1β: Interleukin 1 beta, LPO: Lipid peroxidation, MDA: Malondialdehyde, NADPH: Nicotinamide adenine dinucleotide phosphate, PMS: post mitochondrial supernatant, SE: Status epilepticus, SEM: Standard error of the mean, SOD Superoxide dismutase, TBA: Thiobarbituric acid, TBARS: Thiobarbituric acid reactive substance, TLE: Temporal lobe epilepsy, TNF-α: Tumor necrosis factor alpha

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“…Naringenin (3), a dietary flavonoid prevalent in the peels of citrus fruit, has various biological actions such as a cognitive enhancer [ 48 ] and inhibits monoamine oxidase activity [ 49 ] and neuroprotection [ 50 ]. Likewise, naringenin was found to display antidepressant effects [ 51 ].…”

Section: Resultsmentioning

confidence: 99%

Antidepressant Flavonoids and Their Relationship with Oxidative Stress

Hrițcu

Ionita

Postu

et al. 2017

Oxidative Medicine and Cellular Longevity

106

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Depression is a serious disorder that affects hundreds of millions of people around the world and causes poor quality of life, problem behaviors, and limitations in activities of daily living. Therefore, the search for new therapeutic options is of high interest and growth. Research on the relationship between depression and oxidative stress has shown important biochemical aspects in the development of this disease. Flavonoids are a class of natural products that exhibit several pharmacological properties, including antidepressant-like activity, and affects various physiological and biochemical functions in the body. Studies show the clinical potential of antioxidant flavonoids in treating depressive disorders and strongly suggest that these natural products are interesting prototype compounds in the study of new antidepressant drugs. So, this review will summarize the chemical and pharmacological perspectives related to the discovery of flavonoids with antidepressant activity. The mechanisms of action of these compounds are also discussed, including their actions on oxidative stress relating to depression.

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Neuroprotective role of naringenin on carbaryl induced neurotoxicity in mouse neuroblastoma cells

Cited by 35 publications

References 19 publications

On the Neuroprotective Effects of Naringenin: Pharmacological Targets, Signaling Pathways, Molecular Mechanisms, and Clinical Perspective

On the Neuroprotective Effects of Naringenin: Pharmacological Targets, Signaling Pathways, Molecular Mechanisms, and Clinical Perspective

Effect of naringenin (A naturally occurring flavanone) against pilocarpine-induced status epilepticus and oxidative stress in mice

Antidepressant Flavonoids and Their Relationship with Oxidative Stress

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