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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

Putative nootropic mechanisms of honey and its polyphenols. Calcium influx via the N-methyl-D-aspartate receptor (NMDAR) occurs during the initial phase of NMDAR-dependent LTP. The inductive phase follows CREB phosphorylation through MAPK/ERKs signaling, which ultimately leads to the transcriptional regulation of synaptic plasticity-related proteins. Metabotropic receptors include ligand-gated ion channels that promote calcium influx (AMPA receptor) and enzyme-coupled receptors (such as cholinergic, glutamate, and dopamine receptors) that can trigger a second messenger (cAMP/cGMP) to activate downstream effector enzymes. The effector enzymes finally modulate the activation of CREB [123–128]. Honey polyphenols (HP: luteolin, myricetin, catechin) modulate synaptic plasticity through the activation of CREB by MAPK/ERKs and/or PKA-involved cellular signaling.
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fig2: Putative nootropic mechanisms of honey and its polyphenols. Calcium influx via the N-methyl-D-aspartate receptor (NMDAR) occurs during the initial phase of NMDAR-dependent LTP. The inductive phase follows CREB phosphorylation through MAPK/ERKs signaling, which ultimately leads to the transcriptional regulation of synaptic plasticity-related proteins. Metabotropic receptors include ligand-gated ion channels that promote calcium influx (AMPA receptor) and enzyme-coupled receptors (such as cholinergic, glutamate, and dopamine receptors) that can trigger a second messenger (cAMP/cGMP) to activate downstream effector enzymes. The effector enzymes finally modulate the activation of CREB [123–128]. Honey polyphenols (HP: luteolin, myricetin, catechin) modulate synaptic plasticity through the activation of CREB by MAPK/ERKs and/or PKA-involved cellular signaling.

Mentions: Current research has clarified only a portion of the involvement of honey polyphenols in memory-related signaling pathways. However, the overall body of knowledge clearly suggests the neuroprotective roles of honey and several supplementary experimental studies support its memory-improving effects. Overall, honey or its bioactive constituents might influence multiple signaling pathways to exert its memory-improving effects (Figure 2).


Neurological effects of honey: current and future prospects.

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

Putative nootropic mechanisms of honey and its polyphenols. Calcium influx via the N-methyl-D-aspartate receptor (NMDAR) occurs during the initial phase of NMDAR-dependent LTP. The inductive phase follows CREB phosphorylation through MAPK/ERKs signaling, which ultimately leads to the transcriptional regulation of synaptic plasticity-related proteins. Metabotropic receptors include ligand-gated ion channels that promote calcium influx (AMPA receptor) and enzyme-coupled receptors (such as cholinergic, glutamate, and dopamine receptors) that can trigger a second messenger (cAMP/cGMP) to activate downstream effector enzymes. The effector enzymes finally modulate the activation of CREB [123–128]. Honey polyphenols (HP: luteolin, myricetin, catechin) modulate synaptic plasticity through the activation of CREB by MAPK/ERKs and/or PKA-involved cellular signaling.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig2: Putative nootropic mechanisms of honey and its polyphenols. Calcium influx via the N-methyl-D-aspartate receptor (NMDAR) occurs during the initial phase of NMDAR-dependent LTP. The inductive phase follows CREB phosphorylation through MAPK/ERKs signaling, which ultimately leads to the transcriptional regulation of synaptic plasticity-related proteins. Metabotropic receptors include ligand-gated ion channels that promote calcium influx (AMPA receptor) and enzyme-coupled receptors (such as cholinergic, glutamate, and dopamine receptors) that can trigger a second messenger (cAMP/cGMP) to activate downstream effector enzymes. The effector enzymes finally modulate the activation of CREB [123–128]. Honey polyphenols (HP: luteolin, myricetin, catechin) modulate synaptic plasticity through the activation of CREB by MAPK/ERKs and/or PKA-involved cellular signaling.
Mentions: Current research has clarified only a portion of the involvement of honey polyphenols in memory-related signaling pathways. However, the overall body of knowledge clearly suggests the neuroprotective roles of honey and several supplementary experimental studies support its memory-improving effects. Overall, honey or its bioactive constituents might influence multiple signaling pathways to exert its memory-improving effects (Figure 2).

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