Neurobiological effects of gallic acid: current perspectives

Abstract

Gallic acid (GA) is a phenolic molecule found naturally in a wide range of fruits as well as in medicinal plants. It has many health benefits due to its antioxidant properties. This study focused on finding out the neurobiological effects and mechanisms of GA using published data from reputed databases. For this, data were collected from various sources, such as PubMed/Medline, Science Direct, Scopus, Google Scholar, SpringerLink, and Web of Science. The findings suggest that GA can be used to manage several neurological diseases and disorders, such as Alzheimer's disease, Parkinson's disease, strokes, sedation, depression, psychosis, neuropathic pain, anxiety, and memory loss, as well as neuroinflammation. According to database reports and this current literature-based study, GA may be considered one of the potential lead compounds to treat neurological diseases and disorders. More preclinical and clinical studies are required to establish GA as a neuroprotective drug.

Keywords: Brain health; Gallic acid; neuroprotective activity; pharmacological effects; Molecular mechanisms.

Fig. 1

Chemical structure of gallic acid (3,4,5-trihydroxy benzoic acid)

Fig. 2

Schematic representation of the possible action pathways of gallic acid in Alzheimer’s disease. Abbreviations and symbols: ↑ increase, ↓decrease, GA gallic acid, BACE1 beta secretase-1, κ-CN kappa-casein, Aβ amyloid beta, ROS reactive oxygen species, ChEt cholinergic transmitter, ChEs cholinesterase, NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells

Fig. 3

Possible anti-Parkinson mechanism of gallic acid

Fig. 4

Anxiolytic and memory enhancing pathways of gallic acid. ↑ increase, ↓decrease, GA gallic acid, ROS reactive oxygen species, TCA tricarboxylic acid, MDA malondialdehyde, 5HT_1A 5-hydroxytryptamine (serotonin) receptor 1A, PN plasma nitrite, Nos nitric oxide synthase, CoS corticosterone, iNOs Inducible nitric oxide synthase, LPO lipid peroxidation, GSH glutathione, HIP hippocampus

Fig. 5

Gallic acid against depression: possible molecular interaction. ↑ increase; ↓decrease, GA gallic acid, DP dopamine, 5HT serotonin, ADN adrenaline, MAO-A Monoamine oxidase A, MDA malondialdehyde, CAT catalase, HPO hydrogen peroxide, ROS reactive oxygen species, M/A-1 MAO-A inhibition, M-/A-2 antioxidant response

Fig. 6

Overall neurological activities of gallic acid against different diseases and states of different mediators or proteins. ↑increase, ↓decrease. Aβ amyloid β protein, TNF- α tumour necrosis factor-α, TBARS 2-thiobarbituric acid reactive substances, κ-CN kappa-casein, NF-kB nuclear factor kappa B, GSH glutathione, MDA malondialdehyde, TCA tricarboxylic acid, 5-HT_1A 5-hydroxytryptamine (serotonin) receptor 1A, DP dopamine, AChE acetylcholinesterase, GABA gamma-aminobutyric acid, COX-2: cyclooxygenase-2, IL-6 interleukin-6, IL-10 interleukin-10, IL-1β interleukin-1β, ROS reactive oxygen species, MPO myeloperoxidase, RIPK-1 receptor-interacting protein kinase-1, RIPK-3 receptor-interacting protein kinase-3,NO nitric oxide, iNOS inducible nitric oxide synthase, LPO lipid peroxidation, MCP1 monocyte chemoattractant protein-1, HPO hydrogen peroxide, AND adrenaline; PN plasma nitrile, NOS nitric oxide synthase, CoS corticosterone