A Mechanistic Evaluation of Antioxidant Nutraceuticals on Their Potential against Age-Associated Neurodegenerative Diseases

Ramli, Nur Zuliani; Yahaya, Mohamad Fairuz; Tooyama, Ikuo; Damanhuri, Hanafi Ahmad

doi:10.3390/antiox9101019

Cited by 28 publications

(14 citation statements)

References 237 publications

(258 reference statements)

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“…Furthermore, it also reduces the expression of tumor necrosis factor-α (TNF-α), an important inflammatory cytokine. Collectively, MLT shows defense against inflammatory properties [3,89]. The pro-inflammatory agent TNF-α induces pathological conditions such as chronic inflammation and malignancy [90].…”

Section: Melatonin As An Anti-inflammatory Agentmentioning

confidence: 99%

The promising oncostatic effects of melatonin against ovarian cancer

Das

Samanta

2021

World Journal of Current Med and Pharm Research

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Melatonin is a pineal hormone, secreted at the subjective night. It is involved in the regulation of many physiological functions, including the sleep-wake cycle, gonadal activity, free radical scavenging, immunomodulation, neuro-protection, and cancer progression. Melatonin acts through cell surface receptors (MT1 and MT2) as well as nuclear receptors. Circadian dysfunction can alter the secretion of melatonin. Inappropriate melatonin level promotes the initiation of many pathologies including cancer. Ovarian cancer is a common form of gynecological disease. Several studies indicate the profound link between impaired melatonin secretion and the progression of ovarian cancer. Melatonin exerts oncostatic effects in multiple ways; it acts as a potent antioxidant, induces apoptosis, and regulates metabolism, and chronic inflammatory response in ovarian cancer cells. Moreover, melatonin improves the efficacy of the current treatment regimen of ovarian cancer and can be used as an adjuvant.

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Section: Melatonin As An Anti-inflammatory Agentmentioning

confidence: 99%

The promising oncostatic effects of melatonin against ovarian cancer

Das

Samanta

2021

World Journal of Current Med and Pharm Research

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“…Oxidative stress resulting from an imbalance in cellular redox can occur due to the production of excessive levels of reactive oxygen species (ROS) and/or a deficit of cellular antioxidant systems. Supplementation with various classes of antioxidants has been widely investigated for neurodegenerative diseases (for recent reviews, see [ 1 , 2 ]). Excess levels of ROS can occur from inflammatory responses by innate immune cells (e.g., neutrophils, monocytes/macrophages/microglia) due to infections or chronic autoimmune responses [ 2 ], deficiencies in mitochondrial oxidative phosphorylation pathways [ 3 , 4 ], and environmental factors such as UV light, toxic chemicals, or heavy metals.…”

Section: Introductionmentioning

confidence: 99%

Thioredoxin-Interacting Protein (TXNIP) with Focus on Brain and Neurodegenerative Diseases

Tsubaki

Tooyama

Walker

2020

IJMS

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The development of new therapeutic approaches to diseases relies on the identification of key molecular targets involved in amplifying disease processes. One such molecule is thioredoxin-interacting protein (TXNIP), also designated thioredoxin-binding protein-2 (TBP-2), a member of the α-arrestin family of proteins and a central regulator of glucose and lipid metabolism, involved in diabetes-associated vascular endothelial dysfunction and inflammation. TXNIP sequesters reduced thioredoxin (TRX), inhibiting its function, resulting in increased oxidative stress. Many different cellular stress factors regulate TXNIP expression, including high glucose, endoplasmic reticulum stress, free radicals, hypoxia, nitric oxide, insulin, and adenosine-containing molecules. TXNIP is also directly involved in inflammatory activation through its interaction with the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome complex. Neurodegenerative diseases such as Alzheimer’s disease have significant pathologies associated with increased oxidative stress, inflammation, and vascular dysfunctions. In addition, as dysfunctions in glucose and cellular metabolism have been associated with such brain diseases, a role for TXNIP in neurodegeneration has actively been investigated. In this review, we will focus on the current state of the understanding of possible normal and pathological functions of TXNIP in the central nervous system from studies of in vitro neural cells and the brains of humans and experimental animals with reference to other studies. As TXNIP can be expressed by neurons, microglia, astrocytes, and endothelial cells, a complex pattern of regulation and function in the brain is suggested. We will examine data suggesting TXNIP as a therapeutic target for neurodegenerative diseases where further research is needed.

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“…Antioxidant compounds have been used to protect neurons against different type of damage [27][28][29][30]. Among them, apocynin (4-hidroxy-3-methoxyacetophenone) is one of the most frequently used as an NADPH oxidase inhibitor.…”

Section: Introductionmentioning

confidence: 99%

Apocynin Prevents Anxiety-Like Behavior and Histone Deacetylases Overexpression Induced by Sub-Chronic Stress in Mice

et al. 2021

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Anxiety disorders are common mental health diseases affecting up to 7% of people around the world. Stress is considered one of the major environmental risk factors to promote anxiety disorders through mechanisms involving epigenetic changes. Moreover, alteration in redox balance and increased reactive oxygen species (ROS) production have been detected in anxiety patients and in stressed-animal models of anxiety. Here we tested if the administration of apocynin, a natural origin antioxidant, may prevent the anxiety-like phenotype and reduction of histone acetylation induced by a subchronic forced swimming stress (FSS) paradigm. We found that apocynin prevented the enhanced latency time in the novelty-suppressed feeding test, and the production of malondialdehyde induced by FSS. Moreover, apocynin was able to block the upregulation of p47phox, a key subunit of the NADPH oxidase complex. Finally, apocynin prevented the rise of hippocampal Hdac1, Hdac4 and Hdac5, and the reduction of histone-3 acetylation levels promoted by FSS exposure. In conclusion, our results provide evidence that apocynin reduces the deleterious effect of stress and suggests that oxidative stress may regulate epigenetic mechanisms.

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A Mechanistic Evaluation of Antioxidant Nutraceuticals on Their Potential against Age-Associated Neurodegenerative Diseases

Cited by 28 publications

References 237 publications

The promising oncostatic effects of melatonin against ovarian cancer

The promising oncostatic effects of melatonin against ovarian cancer

Thioredoxin-Interacting Protein (TXNIP) with Focus on Brain and Neurodegenerative Diseases

Apocynin Prevents Anxiety-Like Behavior and Histone Deacetylases Overexpression Induced by Sub-Chronic Stress in Mice

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