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Neurological effects of honey: current and future prospects.

Mijanur Rahman M, Gan SH, Khalil MI - Evid Based Complement Alternat Med (2014)

Bottom Line: Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities.Honey polyphenols are useful in improving memory deficits and can act at the molecular level.Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka 1342, Bangladesh.

ABSTRACT
Honey is the only insect-derived natural product with therapeutic, traditional, spiritual, nutritional, cosmetic, and industrial value. In addition to having excellent nutritional value, honey is a good source of physiologically active natural compounds, such as polyphenols. Unfortunately, there are very few current research projects investigating the nootropic and neuropharmacological effects of honey, and these are still in their early stages. Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities. Research suggests that the polyphenol constituents of honey can quench biological reactive oxygen species and counter oxidative stress while restoring the cellular antioxidant defense system. Honey polyphenols are also directly involved in apoptotic activities while attenuating microglia-induced neuroinflammation. Honey polyphenols are useful in improving memory deficits and can act at the molecular level. Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.

No MeSH data available.


Related in: MedlinePlus

The putative neuroprotective mechanism of honey and its polyphenols. The generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. The dysfunction of the antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. The ultimate outcome of such oxidative stress is neuronal cell death through an inflammatory, apoptotic, or necrotic response [111–114, 116, 119]. Honey (H) and its polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death by attenuating neuroinflammation and apoptosis. However, the neuroinflammatory responses overlap with apoptosis, and the role of honey in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.
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Related In: Results  -  Collection


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fig1: The putative neuroprotective mechanism of honey and its polyphenols. The generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. The dysfunction of the antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. The ultimate outcome of such oxidative stress is neuronal cell death through an inflammatory, apoptotic, or necrotic response [111–114, 116, 119]. Honey (H) and its polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death by attenuating neuroinflammation and apoptosis. However, the neuroinflammatory responses overlap with apoptosis, and the role of honey in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.

Mentions: Much research over the last few decades has established nutraceuticals as neuroprotective agents. In addition to the acute modulation of the antioxidant defense system, several nutraceuticals can also modulate gene expression to confer long-term protection [115, 116]. Phytochemicals can also modify cellular behaviors by influencing receptor function as well as by modulating intracellular events, such as cell-signaling cascades [117, 118]. Honey and its constituents can ameliorate oxidative stress and oxidative stress-related effects. The neuroprotective effects of honey are exerted at different stages of neurodegeneration and play prominent roles in early events (Figure 1).


Neurological effects of honey: current and future prospects.

Mijanur Rahman M, Gan SH, Khalil MI - Evid Based Complement Alternat Med (2014)

The putative neuroprotective mechanism of honey and its polyphenols. The generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. The dysfunction of the antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. The ultimate outcome of such oxidative stress is neuronal cell death through an inflammatory, apoptotic, or necrotic response [111–114, 116, 119]. Honey (H) and its polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death by attenuating neuroinflammation and apoptosis. However, the neuroinflammatory responses overlap with apoptosis, and the role of honey in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020454&req=5

fig1: The putative neuroprotective mechanism of honey and its polyphenols. The generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) increases irrespective of neurodamaging insults that lead to oxidative stress. The dysfunction of the antioxidant defense system synergistically causes reactive species accumulation, leading to oxidative stress. The ultimate outcome of such oxidative stress is neuronal cell death through an inflammatory, apoptotic, or necrotic response [111–114, 116, 119]. Honey (H) and its polyphenol constituents (HP) can counter oxidative stress by limiting the generation of reactive species as well as by strengthening the cellular antioxidant defense system. Honey and several honey polyphenols (apigenin, ferulic acid, and catechin) prevent neuronal cell death by attenuating neuroinflammation and apoptosis. However, the neuroinflammatory responses overlap with apoptosis, and the role of honey in necrotic cell death remains unclear. X = stop or prevent and + = improve or intensify.
Mentions: Much research over the last few decades has established nutraceuticals as neuroprotective agents. In addition to the acute modulation of the antioxidant defense system, several nutraceuticals can also modulate gene expression to confer long-term protection [115, 116]. Phytochemicals can also modify cellular behaviors by influencing receptor function as well as by modulating intracellular events, such as cell-signaling cascades [117, 118]. Honey and its constituents can ameliorate oxidative stress and oxidative stress-related effects. The neuroprotective effects of honey are exerted at different stages of neurodegeneration and play prominent roles in early events (Figure 1).

Bottom Line: Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities.Honey polyphenols are useful in improving memory deficits and can act at the molecular level.Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Biology, Jahangirnagar University, Savar, Dhaka 1342, Bangladesh.

ABSTRACT
Honey is the only insect-derived natural product with therapeutic, traditional, spiritual, nutritional, cosmetic, and industrial value. In addition to having excellent nutritional value, honey is a good source of physiologically active natural compounds, such as polyphenols. Unfortunately, there are very few current research projects investigating the nootropic and neuropharmacological effects of honey, and these are still in their early stages. Raw honey possesses nootropic effects, such as memory-enhancing effects, as well as neuropharmacological activities, such as anxiolytic, antinociceptive, anticonvulsant, and antidepressant activities. Research suggests that the polyphenol constituents of honey can quench biological reactive oxygen species and counter oxidative stress while restoring the cellular antioxidant defense system. Honey polyphenols are also directly involved in apoptotic activities while attenuating microglia-induced neuroinflammation. Honey polyphenols are useful in improving memory deficits and can act at the molecular level. Therefore, the ultimate biochemical impact of honey on specific neurodegenerative diseases, apoptosis, necrosis, neuroinflammation, synaptic plasticity, and behavior-modulating neural circuitry should be evaluated with appropriate mechanistic approaches using biochemical and molecular tools.

No MeSH data available.


Related in: MedlinePlus