Table 1 Overview of the effects of gallic acid in neurological diseases and disorders
From: Neurobiological effects of gallic acid: current perspectives
Neurological disease | Experimental model | Concentration/Doses | Effects/Mechanisms | References |
|---|---|---|---|---|
Alzheimer’s disease | Wistar rats (aluminium-chloride induced AD), in vivo | 100 mg/kg b.w | ↓CAT, ↓GSH, ↓SOD, ↓serum electrolyte, ↓neurotransmitter levels, ↑MDA, ↑ H2O2 and ↑NO | [115] |
Drosophila melanogaster BL#33,798 cultures, in vitro | IC50 = 50—100 µM | ↓ Aβ, ↓ ChEs, ↓BACE-1 | [116] | |
APPswe/PS1dE9 transgenic mice (capable of Aβ plaque deposition at the age of 4 months), in vivo | 30 mg/kg b.w | ↓neurotoxicity, ↓ Aβ1–42 | [187] | |
Rats (AD induced through Aβ hippocampal injection), in vivo | 50, 100, and 200 mg/kg b.w | ↑cognitive function, ↓neural damage ↓Aβ plaques | [60] | |
Rats (i.p. injection of trimethyltin, 8 mg/kg b.w.), in vivo | 50 and 100 mg/kg b.w | ↑ BDNF hippocampal level > TMT group > ↓ TNF-α hippocampal level | [15] | |
Rats (intracerebroventricular–STZ injection), in vivo | 30 mg/kg b.w | ↑the passive avoidance, ↑memory ↑SOD, ↑GPx, ↑CAT, ↓TBARS | [104] | |
Heochromocytoma 12 cells, in vitro | IC50 = 3.7 ± 0.3 µM | ↓neurotoxicity ↓κ-CN activity, ↓Aβ peptide fibril | [96] | |
Microglial, neuronal cells, in vitro | IC50 = 5–50 μM | ↓ cytokines, ↓NF-kB, ↓neurotoxicity | [85] | |
Mice, (Aβ 142 and Aβ 421 were administered by intracerebroventricular (ICV) injection), in vivo | 10 and 30 mg/kg b.w | ↓cognitive dysfunction, ↓ Aβ, ↓cytokines, ↓neuronal cell death | ||
Parkinson’s disease | Wistar male rats (catatonia induced by PPZ), in vivo | 100, 200, 400 and 600 mg/kg b.w. (i.p) | ↓catatonic responses | [67] |
SH-SY5Y cells, in vitro | IC50 = 0.25–2.5 μg/ml | ↓neuronal cells damage, ↓ROS, ↓Keap-1, ↓caspase-3 ↓BDNF, ↓Nrf2, ↓p-CREB | [27] | |
Rats received reserpine, in vivo | Dose = 13.5—40.5 mg/kg/day b.w | ↓vacuous chewing movements | [134] | |
Rats (PD induced through 6-OHDA; 8 μg/2 μL injected into the medial forebrain bundle), in vivo | Dose = 50, 100, and 200 mg/kg b.w | ↑ memory ↑GPx, ↓ TBARS | [103] | |
Rats (PD induced by apomorphine), in vivo | 200 mg kg b.w | ↓motor dysfunctions,↓ ROS and↓ gamma wave power, | [141] | |
Rats, (tacrine 2.5 mg/kg b.w, i.p.), in vivo | 150 mg/kg b.w | ↓vacuous chewing movements | [81] | |
Mice, (Haloperidol 1 mg/kg b.w, i.p.), in vivo | ↓catalepsy | |||
Anxiety | Rats (HE mediated by bile duct ligation (BDL and NOR, open field and Morris water maze test), in vivo | 20 and 30 mg/kg b.w | ↑memory, ↑ AMPK pathway activity | [71] |
STZ-induced diabetic rats, in vivo | 10, 20, and 40 mg/kg b.w | ↓GSH in hippocampus and prefrontal cortex | [124] | |
Mice acute and chronic stress in vivo | 5, 10, and 20 mg/ kg b.w | ↓serum and brain MDA levels ↑brain TCA | [137] | |
Rats (EPM test), in vivo | 30 and 300 mg/kg b.w | ↑5-HT1A receptor activity ↑time spent and entries in the open arms of elevated plus maze (EPM) | [105] | |
Mice (EPM test), in vivo | GA nanoparticles: 10 mg/kg, 10 mg/kg b.w | ↓plasma nitrite level | [110] | |
Mice stress was generated by immobility, in vivo | 5, 10, and 20 mg/kg b.w | ↓plasma nitrite, ↓corticosterone levels | [42] | |
Depression | Rats anxiety- depression induced by sodium arsenite, in vivo | 50 and 100 mg/kg b.w | ↓immobility duration ↑time spent in open arm and light box | [140] |
Mice post-stroke depression, in vivo | 30 and 60 mg/kg | ↓immobility duration | [25] | |
Mice (TST model), in vivo | 25 and 50 mg/kg b.w | ↓immobility duration | [108] | |
Mice unpredictable chronic mild stress, in vivo | 10 and 20 mg/kg b.w | ↓immobility duration, ↓MDA, ↓MAO-A ↓plasma corticosterone levels | [30] | |
Mice (DST and TST model), in vivo | 10 mg/kg b.w. (GA nanoparticles) | ↓immobility duration ↓ MDA, ↓MAO-A, ↓CAT | [111] | |
Psychosis | Mice (ketamine-induced psychosis), in vivo | 50, 100, and 200 mg/kg, b.w. (p.o) | neuroprotective effects in psychosis ↓ LP, ↓DP,↓TNF-α, ↓AChE ↑ GABA, ↑glutathione | [185] |
Sedation | Rats, in vivo | 500 mg/kg (p.o.) | ↓locomotor activity in rats | [105] |
Strokes | C57BL/6 J mice, (MCAO method), in vivo | 50, 100, and 150 mg/kg b.w. (p.o.) | ↓ brain edema, neuroprotective, ↑ the integrity of the BBB, ↓ ischemic brain injury, ↓iNOS, ↓MCP-1, ↓COX-2 ↑Arg-1, ↑IL-10, ↑CD206 | [128] |
Rats (focal cerebral ischemia: MCAO), in vivo | 25, 37.5, and 50Â mg/kg b.w | (-) unknown effects | [164] | |
Human SH-SY5Y neuroblastoma cells, in vitro | IC50 = 0.1—1 μM | ↓ ROS, ↓apoptosis ↓mitochondrial dysfunction ↓hypoxia,↑reoxygenation ↑protection from cerebral ischemia/reperfusion injury | ||
Rats (permanent cerebral hypo-perfusion), in vivo | 100 mg/kg b.w. (p.o.) | ↑spatial memory performance ↑MDA ↓cognitive deficits through the elevation of cerebral antioxidant defense ↑activity against 2-vessel occlusion (2VO) | [87] | |
Rats (permanent cerebral hypo-perfusion), in vivo | 100 mg/kg b.w. (p.o.) | ↑ flourished passive avoidance of memory, LTP in the HIP, and cell survival in the HIP and cortex of ischemic rats | [142] | |
Rats (transient cerebral hypo-perfusion), in vivo | 50, 100, and 200 mg/kg b.w. (p.o.) | ↑antioxidant defense against BCCA occlusion ↑neuroprotection | [49] | |
Neuropathic pain | Mice (pain developed by paclitaxel: 2 mg/kg, i.p.), in vivo | 20 and 40 mg/kg b.w | ↓ TNF-α, ↓Ca2+, ↓TBARS, ↓superoxide anion, ↓GSH, ↓MPO, ↓ thermal and mechanical hyperalgesia | [82] |
Brain tumor/Cerebral Glioblastoma | DBTRG-05MG human glioblastoma cells, in vitro | IC50 = 20—40 µM | ↑Ca2+ ↑phospholipase C-dependent release from the ER ↑ROS, ↑apoptosis, ↑cytotoxicity | [68] |
T98G human glioblastoma cell lines, in vitro | IC50 = 100 µg/ml | ↑miR-421 regulation of the cell cycle S-phase ↑serine/ threonine protein kinase ↑DNA damage ↑cell cycle arrest at the G1-S and S phases ↑apoptosis, ↑cytotoxicity | [119] | |
U87, U251 human glioma cells, in vitro | IC50 = 20 μg/ml | ↓glioma cells viability, ↓proliferation, ↓invasion, ↓angiogenesis, ↑cytotoxicity | [98] | |
Neuroinflammation | Sprague Dawley rats (neuroinflammation induced by intranigral infusion of LPS), in vivo | 50 and 100 mg/kg b.w. (p.o.) | ↓ iNOS, ↓IL-1β, ↓heme oxygenase-1 level, ↓α-synuclein aggregation, ↓caspase 3,↓ RIPK-1, ↓RIPK-3 levels, ↓ROS, ↓apoptosis | [95] |
LPS-treated BV2 microglial cells, in vitro | IC50 = 25– 100 μM | ↓NO levels,↓ iNOS expression | ||
Hippocampal neurons co-cultured with glial cells, (LPC-induced inflammation), in vitro | IC50 = 1.0 µM | ↓NF-κB, ↓COX-2, ↓tenascin-C, ↓chondroitin sulfate proteoglycans and ↓glial fibrillary acidic protein | [156] | |
Wistar rats (traumatic brain injury by Marmarou’s method), in vivo | 100 mg/kg b.w. (p.o) | ↓IL-1β, ↓IL-6, and ↓TNF-α | [142] | |
BV-2 cells and Neuro-2A cells (treated by oligomeric Aβ), in vitro | IC50 = 5–50 µM | ↓iNOS, ↓IL-1β, ↓COX-2, and ↓NF-kB | [85] |