Flavonoids and Anthranquinones as Xanthine Oxidase and Monoamine Oxidase Inhibitors: A New Approach Towards Inflammation and Oxidative Stress

Malik, Neelam; Dhiman, Priyanka; Sobarzo‐Sánchez, Eduardo; Khatkar, Anurag

doi:10.2174/1568026619666181120143050

Cited by 19 publications

(11 citation statements)

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“…Flavonoids increase ROS-removing enzymes (SOD, catalase, glutathione reductase) via activation of Keap1 (Kelch ECH-associated protein 1)/Nrf2/ARE (antioxidant responsive element) signaling pathway. Polyphenols (apigenin, catechin, kaempferol, luteolin, quercetin, curcumin) inhibit ROS-producing XO (xanthine oxidase), MAO, and NADPH oxidase (NOX) [53,54,55].…”

Section: Polyphenols Modulate Mitochondrial Function and Exhibit Nmentioning

confidence: 99%

Mitochondria in Neuroprotection by Phytochemicals: Bioactive Polyphenols Modulate Mitochondrial Apoptosis System, Function and Structure

Naoi

Shamoto-Nagai

et al. 2019

IJMS

114

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In aging and neurodegenerative diseases, loss of distinct type of neurons characterizes disease-specific pathological and clinical features, and mitochondria play a pivotal role in neuronal survival and death. Mitochondria are now considered as the organelle to modulate cellular signal pathways and functions, not only to produce energy and reactive oxygen species. Oxidative stress, deficit of neurotrophic factors, and multiple other factors impair mitochondrial function and induce cell death. Multi-functional plant polyphenols, major groups of phytochemicals, are proposed as one of most promising mitochondria-targeting medicine to preserve the activity and structure of mitochondria and neurons. Polyphenols can scavenge reactive oxygen and nitrogen species and activate redox-responsible transcription factors to regulate expression of genes, coding antioxidants, anti-apoptotic Bcl-2 protein family, and pro-survival neurotrophic factors. In mitochondria, polyphenols can directly regulate the mitochondrial apoptosis system either in preventing or promoting way. Polyphenols also modulate mitochondrial biogenesis, dynamics (fission and fusion), and autophagic degradation to keep the quality and number. This review presents the role of polyphenols in regulation of mitochondrial redox state, death signal system, and homeostasis. The dualistic redox properties of polyphenols are associated with controversial regulation of mitochondrial apoptosis system involved in the neuroprotective and anti-carcinogenic functions. Mitochondria-targeted phytochemical derivatives were synthesized based on the phenolic structure to develop a novel series of neuroprotective and anticancer compounds, which promote the bioavailability and effectiveness. Phytochemicals have shown the multiple beneficial effects in mitochondria, but further investigation is required for the clinical application.

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Section: Polyphenols Modulate Mitochondrial Function and Exhibit Nmentioning

confidence: 99%

Mitochondria in Neuroprotection by Phytochemicals: Bioactive Polyphenols Modulate Mitochondrial Apoptosis System, Function and Structure

Naoi

Shamoto-Nagai

et al. 2019

IJMS

114

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“…5-Hydroxyindoleacetate is a downstream metabolite of serotonin converted by monoamine oxidase (MAO) to aldehyde dehydrogenase (ALDH) (Malik, Dhiman, Sobarzo-Sanchez, & Khatkar, 2018), then transformed by acetyl serotonin O-methyltransferase and involved in the synthesis of human melatonin (Botros, Legrand, Pagan, Bondet, & Bourgeron, 2012). Studies that have analyzed the relationship between HUM and 5-hydroxytryptamine have demonstrated that inhibiting the activity of MAO results in anti-inflammation and antioxidation.…”

Section: Discussionmentioning

confidence: 99%

Studies on effect of Tongfengxiaofang in HUM model mice using a UPLC–ESI–Q‐TOF/MS metabolomic approach

Chen

Wang²,

et al. 2021

Biomedical Chromatography

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Hyperuricemia (HUM) is a major risk factor for the development of gout. The traditional Chinese medicine (TCM) complex prescription Tongfengxiaofang (TFXF) is composed of a variety of TCMs. To study the therapeutic effect of TFXF on HUM mice and the mechanisms by which it exerts a therapeutic effect, the biochemical indices were measured and qPCR technique was used. In addition, plasma metabolomics analysis was carried out based on UPLC-Q-TOF/MS to evaluate the characteristics of the metabolic spectrum changes. TFXF significantly downregulated the contents of uric acid, urea nitrogen and creatinine in serum and the concentration of xanthine oxidase in liver of HUM mice. In addition, TFXF significantly inhibited the overexpression of uric acid transporter 1 and glucose transporter 9 and upregulated the expression of organic anion transporter 1 in the kidney. A total of 152 metabolites were identified and 11 key biomarkers were further selected from these pathways to understand the mechanism of TFXF on the arginine biosynthesis, galactose metabolism, pyrimidine metabolism, glycerophospholipid metabolism, tryptophan metabolism and the citrate cycle (TCA cycle). The results of this confirmed the effect of TFXF on HUM and revealed the metabolic activity mechanism.

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“…The basal level of xanthine oxidase is low, its expression is upregulated under I/R conditions. Xanthine oxidase stimulates redundant ROS production, which can lead to oxidative stress injury (Malik et al, 2018). In addition, xanthine oxidase has been shown to play a role in atrial remolding induced by oxidative stress in alloxan-induced diabetic rabbits (Figure 4; Yang et al, 2018).…”

Section: Inhibition Of Xanthine Oxidasementioning

confidence: 99%

Protective Mechanisms of Quercetin Against Myocardial Ischemia Reperfusion Injury

Zhang

Wang

2020

Front. Physiol.

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Quercetin has attracted more attention in recent years due to its protective role against ischemia/reperfusion injury. Quercetin can alleviate oxidative stress injury through the inhibition of NADPH oxidase and xanthine oxidase, blockage of the Fenton reaction, and scavenging of reactive oxygen species. Quercetin can also exert anti-inflammatory and anti-apoptotic effects by reducing the response to inflammatory factors and inhibiting cell apoptosis. Moreover, it can induce vasodilation effects through the inhibition of endothelin-1 receptors, the enhancement of NO stimulation and the activation of the large-conductance calcium-activated potassium channels. Finally, Quercetin can also antagonize the calcium overload. These multifaceted activities of Quercetin make it a potential therapeutic alternative for the treatment of ischemia/reperfusion injury.

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Flavonoids and Anthranquinones as Xanthine Oxidase and Monoamine Oxidase Inhibitors: A New Approach Towards Inflammation and Oxidative Stress

Cited by 19 publications

References 0 publications

Mitochondria in Neuroprotection by Phytochemicals: Bioactive Polyphenols Modulate Mitochondrial Apoptosis System, Function and Structure

Mitochondria in Neuroprotection by Phytochemicals: Bioactive Polyphenols Modulate Mitochondrial Apoptosis System, Function and Structure

Studies on effect of Tongfengxiaofang in HUM model mice using a UPLC–ESI–Q‐TOF/MS metabolomic approach

Protective Mechanisms of Quercetin Against Myocardial Ischemia Reperfusion Injury

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