The discovery and development of new potential antioxidant agents for the treatment of neurodegenerative diseases

Danta, Chhanda Charan; Piplani, Poonam

doi:10.1517/17460441.2014.942218

Cited by 45 publications

(36 citation statements)

References 114 publications

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“…Currently, AChE inhibitors (AChEI) have proven to be the most viable therapeutic target for symptomatic improvement of AD, as AChEIs enhance neuronal transmission (Loizzo et al, 2008). In addition, antioxidant therapy has also been proven to be successful in improving cognitive function and behavioral deficits in AD animal models (Danta & Piplani, 2014). Based on these observation, it has been hypothesized that natural antioxidants with potent cholinesterase inhibitory activity can act as better drug for the treatment of AD and other age-related neurodegenerative disorders (Zhao & Zhao, 2012).…”

Section: Resultsmentioning

confidence: 99%

In vitroantioxidant and anti-cholinesterase activities ofRhizophora mucronata

Suganthy

Devi

2015

Pharmaceutical Biology

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Context: Rhizophora mucronata Lam. (Rhizophoraceae), commonly known as Asiatic mangrove, has been used traditionally among Asian countries as folk medicine. Objective: This study investigates the cholinesterase inhibitory potential and antioxidant activities of R. mucronata. Materials and method: Rhizophora mucronata leaves were successively extracted using solvents of varying polarity and a dosage of 100-500 mg/ml were used for each assay. Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inhibitory activities were assessed according to the method of Ellman. In vitro antioxidant activity was assessed using free radical scavenging, reducing power, and metal-chelating activity (duration -3 months). Total phenolic and flavonoid content were quantified spectrophotometrically. Compound characterization was done using column chromatography, NMR, FTIR, and LC-MS analysis. Results: Methanolic leaf extract (500 mg/ml) exhibited the highest inhibitory activity against AChE (92.73 ± 0.54%) and BuChE (98.98 ± 0.17%), with an IC 50 value of 59.31 ± 0.35 and 51.72 ± 0.33 mg/ml, respectively. Among the different solvent extracts, methanolic extract exhibited the highest antioxidant activity with an IC 50 value of 47.39 ± 0.43, 401.45 ± 18.52, 80.23 ± 0.70, and 316.47 ± 3.56 mg/ml for DPPH, hydroxyl, nitric oxide radical, and hydrogen peroxide, respectively. Total polyphenolic and flavonoid contents in methanolic extract were observed to be 598.13 ± 1.85 mg of gallic acid equivalent and 48.85 ± 0.70 mg of rutin equivalent/ mg of extract. Compound characterization illustrated (+)-catechin as the bioactive compound responsible for cholinesterase inhibitory and antioxidant activities. Conclusion: The presence of rich source of flavonoids, in particular catechin, might be responsible for its cholinesterase inhibitory and antioxidant activities.

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Section: Resultsmentioning

confidence: 99%

In vitroantioxidant and anti-cholinesterase activities ofRhizophora mucronata

Suganthy

Devi

2015

Pharmaceutical Biology

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“…To date, preclinical ROS scavenging trials lack consistency in demonstrating their beneficial effects [312] despite showing promise in animal studies. The lack of translational success could possibly be due to issues with targeting within the therapeutic window, animal model adequacy, the sample size, and bioavailability [313]. The evidence discussed above supporting a role of NOX in brain injury and neurodegeneration has provided impetus towards examining the therapeutic efficacy of NOX inhibitors in these disorders [73], as this approach may offer the best therapeutic option for treating disorders associated with oxidative stress [314].…”

Section: Introductionmentioning

confidence: 99%

NADPH oxidase in brain injury and neurodegenerative disorders

Merry

Wang

Zhang

et al. 2017

Mol Neurodegeneration

355

309

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Oxidative stress is a common denominator in the pathology of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis, as well as in ischemic and traumatic brain injury. The brain is highly vulnerable to oxidative damage due to its high metabolic demand. However, therapies attempting to scavenge free radicals have shown little success. By shifting the focus to inhibit the generation of damaging free radicals, recent studies have identified NADPH oxidase as a major contributor to disease pathology. NADPH oxidase has the primary function to generate free radicals. In particular, there is growing evidence that the isoforms NOX1, NOX2, and NOX4 can be upregulated by a variety of neurodegenerative factors. The majority of recent studies have shown that genetic and pharmacological inhibition of NADPH oxidase enzymes are neuroprotective and able to reduce detrimental aspects of pathology following ischemic and traumatic brain injury, as well as in chronic neurodegenerative disorders. This review aims to summarize evidence supporting the role of NADPH oxidase in the pathology of these neurological disorders, explores pharmacological strategies of targeting this major oxidative stress pathway, and outlines obstacles that need to be overcome for successful translation of these therapies to the clinic.

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“…While such species are generated in normal physiological conditions, during pathological conditions such as ionizing radiation, UV exposure, inflammation, and the presence of free metal ions (e.g., Cu I/II and Fe II/III ) these highly reactive species are overproduced [1,[4][5][6][7][8][9]. e overproduction of ROS leads to oxidative stress which is associated with aging and the pathogenesis of diseases such as cardiovascular disease, cancer, and several neurodegenerative disorders (e.g., Alzheimer's disease, Parkinson's disease, and ALS) [1,[3][4][5][6][7][8][9][10]. To repair or mediate against oxidative stress cells use antioxidants to scavenge free radicals and maintain a healthy redox balance [1,10,11].…”

Section: Introductionmentioning

confidence: 99%

“…e overproduction of ROS leads to oxidative stress which is associated with aging and the pathogenesis of diseases such as cardiovascular disease, cancer, and several neurodegenerative disorders (e.g., Alzheimer's disease, Parkinson's disease, and ALS) [1,[3][4][5][6][7][8][9][10]. To repair or mediate against oxidative stress cells use antioxidants to scavenge free radicals and maintain a healthy redox balance [1,10,11]. A key antioxidant in eukaryotes is glutathione (GSH) which is a cysteine-based tripeptide [9,10,12,13].…”

Section: Introductionmentioning

confidence: 99%

“…To repair or mediate against oxidative stress cells use antioxidants to scavenge free radicals and maintain a healthy redox balance [1,10,11]. A key antioxidant in eukaryotes is glutathione (GSH) which is a cysteine-based tripeptide [9,10,12,13]. However, GSH is not the only naturally produced antioxidant and several organisms produce other thiol containing antioxidants [14].…”

Section: Introductionmentioning

confidence: 99%

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A Computational Investigation of the Binding of the Selenium Analogues of Ergothioneine and Ovothiol to Cu(I) and Cu(II) and the Effect of Binding on the Redox Potential of the Cu(II)/Cu(I) Redox Couple

Wiebe

Zaliskyy

Bushnell

2019

Journal of Chemistry

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The complexes formed from the binding of ovoselenol (OSeH) and ergoseloneine (ESeH) to Cu(II) and Cu(I) have been investigated with DFT methods. From the calculated thermodynamics, the binding of OSeH and ESeH to Cu(II) and Cu(I) ions increases the reduction potential for the Cu(II)/Cu(I) redox couple. The calculated reduction potentials for the Cu(II)(OSe)2/Cu(I)(OSeH)3+ and Cu(II)(ESe)2/Cu(I)(ESeH)3+ redox couples were found to be 1.15 V and 1.24 V in a dilute aqueous solution. By combining the half reactions for the oxidation of OSeH to the diselenide OSeSeO with the reduction of Cu(II)(OSe)2 to Cu(I)(OSeH)3+, the calculated EMF was 0.90 V. For the oxidation of ESeH to the diselenide ESeSeE with the concomitant reduction of Cu(II)(ESe)2 to Cu(I)(ESeH)3+, the calculated EMF was 0.67 V. Thus, for both systems, the reduction of Cu(II) to Cu(I) with concomitant formation of either diselenide is thermodynamically favourable, and it is expected that both OSeH and ESeH are suitable for the protection against copper induced oxidative damage. As a result, the inhibition of the recycling of Cu(I) to Cu(II) is thermodynamically favourable in the presence of OSeH and ESeH.

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The discovery and development of new potential antioxidant agents for the treatment of neurodegenerative diseases

Cited by 45 publications

References 114 publications

In vitroantioxidant and anti-cholinesterase activities ofRhizophora mucronata

In vitroantioxidant and anti-cholinesterase activities ofRhizophora mucronata

NADPH oxidase in brain injury and neurodegenerative disorders

A Computational Investigation of the Binding of the Selenium Analogues of Ergothioneine and Ovothiol to Cu(I) and Cu(II) and the Effect of Binding on the Redox Potential of the Cu(II)/Cu(I) Redox Couple

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