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Protective effects of curcumin and Ginkgo biloba extract combination on a new model of Alzheimer’s disease

Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative illnesses, and yet, no workable treatments have been discovered to prevent or reverse AD. Curcumin (CUR), the major polyphenolic compound of turmeric (Curcuma longa) rhizomes, and Ginkgo biloba extract (GBE) are natural substanc...

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Published in:Inflammopharmacology 2023-06, Vol.31 (3), p.1449-1464
Main Authors: Assi, Abdel-Azim, Farrag, Magda M. Y., Badary, Dalia M., Allam, Essmat A. H., Nicola, Mariam A.
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description Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative illnesses, and yet, no workable treatments have been discovered to prevent or reverse AD. Curcumin (CUR), the major polyphenolic compound of turmeric (Curcuma longa) rhizomes, and Ginkgo biloba extract (GBE) are natural substances derived from conventional Chinese herbs that have long been shown to provide therapeutic advantages for AD. The uptake of curcumin into the brain is severely restricted by its low ability to cross the blood–brain barrier (BBB). Meanwhile, GBE has been shown to improve BBB permeability. The present study evaluated the neuroprotective effects and pharmacokinetic profile of curcumin and GBE combination to find out whether GBE can enhance curcumin’s beneficial effects in AD by raising its brain concentration. Results revealed that CUR + GBE achieved significantly higher levels of curcumin in the brain and plasma after 30 min and 1 h of oral administration, compared to curcumin alone, and this was confirmed by reversed phase high-performance liquid chromatography (RP-HPLC). The effect of combined oral treatment, for 28 successive days, on cognitive function and other AD-like alterations was studied in scopolamine-heavy metal mixtures (SCO + HMM) AD model in rats. The combination reversed at least, partially on the learning and memory impairment induced by SCO + HMM. This was associated with a more pronounced inhibitory effect on acetylcholinesterase (AChE), caspase-3, hippocampal amyloid beta (Aβ1-42), and phosphorylated tau protein (p-tau) count, and pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukine-1beta (IL-1β), as compared to the curcumin alone-treated group. Additionally, the combined treatment significantly decreased lipid peroxidation (MDA) and increased levels of reduced glutathione (GSH), when compared with the curcumin alone. These findings support the concept that the combination strategy might be an alternative therapy in the management/prevention of neurological disorders. This study sheds light on a new approach for exploring new phyto-therapies for AD and emphasizes that more research should focus on the synergic effects of herbal drugs in future. Graphical abstract
doi_str_mv 10.1007/s10787-023-01164-6
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This was associated with a more pronounced inhibitory effect on acetylcholinesterase (AChE), caspase-3, hippocampal amyloid beta (Aβ1-42), and phosphorylated tau protein (p-tau) count, and pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukine-1beta (IL-1β), as compared to the curcumin alone-treated group. Additionally, the combined treatment significantly decreased lipid peroxidation (MDA) and increased levels of reduced glutathione (GSH), when compared with the curcumin alone. These findings support the concept that the combination strategy might be an alternative therapy in the management/prevention of neurological disorders. This study sheds light on a new approach for exploring new phyto-therapies for AD and emphasizes that more research should focus on the synergic effects of herbal drugs in future. 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H.</creatorcontrib><creatorcontrib>Nicola, Mariam A.</creatorcontrib><title>Protective effects of curcumin and Ginkgo biloba extract combination on a new model of Alzheimer’s disease</title><title>Inflammopharmacology</title><addtitle>Inflammopharmacol</addtitle><addtitle>Inflammopharmacology</addtitle><description>Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative illnesses, and yet, no workable treatments have been discovered to prevent or reverse AD. Curcumin (CUR), the major polyphenolic compound of turmeric (Curcuma longa) rhizomes, and Ginkgo biloba extract (GBE) are natural substances derived from conventional Chinese herbs that have long been shown to provide therapeutic advantages for AD. The uptake of curcumin into the brain is severely restricted by its low ability to cross the blood–brain barrier (BBB). Meanwhile, GBE has been shown to improve BBB permeability. 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This was associated with a more pronounced inhibitory effect on acetylcholinesterase (AChE), caspase-3, hippocampal amyloid beta (Aβ1-42), and phosphorylated tau protein (p-tau) count, and pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and interleukine-1beta (IL-1β), as compared to the curcumin alone-treated group. Additionally, the combined treatment significantly decreased lipid peroxidation (MDA) and increased levels of reduced glutathione (GSH), when compared with the curcumin alone. These findings support the concept that the combination strategy might be an alternative therapy in the management/prevention of neurological disorders. This study sheds light on a new approach for exploring new phyto-therapies for AD and emphasizes that more research should focus on the synergic effects of herbal drugs in future. 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subjects Acetylcholinesterase - metabolism
Allergology
Alzheimer Disease - drug therapy
Amyloid beta-Peptides - metabolism
Animals
Biomedical and Life Sciences
Biomedicine
Blood-Brain Barrier
Curcumin - pharmacokinetics
Curcumin - pharmacology
Curcumin - therapeutic use
Dermatology
Gastroenterology
Ginkgo Extract - pharmacokinetics
Ginkgo Extract - pharmacology
Ginkgo Extract - therapeutic use
Humans
Immunology
Neuroprotective Agents - pharmacokinetics
Neuroprotective Agents - pharmacology
Neuroprotective Agents - therapeutic use
Original
Original Article
Pharmacology/Toxicology
Rats
Rheumatology
title Protective effects of curcumin and Ginkgo biloba extract combination on a new model of Alzheimer’s disease
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