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. 2021 Oct 2;26(19):5985. doi: 10.3390/molecules26195985

Table 1.

Neuropharmacological mechanisms of polydatin against different NDDs.

NDDs Methods Models Neuropharmacological Mechanisms References
AD Chronic cerebral hypoperfusion in vivo: Sprague–Dawley rats ↓MDA, ↑CAT, ↑SOD [44]
Doxorubicin-induced cognitive impairment in vivo: Sprague–Dawley rats ↓Nrf2, ↑NF-κB, ↓caspase-3, ↓caspase-9 [45,46]
HIBI in vivo: Sprague–Dawley rats ↓Memory deficient, ↑BDNF [47]
Chronic ethanol exposure in vivo: Sprague–Dawley rats ↑Cell survival, ↓cdk5, ↓functional defects [48]
Polymerization of Aβ in vitro: Aβ25–35 ↓Aβ25–35 polymerization [49,50]
D-galactose-induced in vitro: DPPH
in vivo: Male Kunming mice
↑Body weight, ↓MDA, ↑CAT, ↑SOD, ↑GSH, ↓IL-1β, ↓TNF-α, ↓IL-6, ↓ Bax/Bcl-2, ↓caspase-3 [30]
PD Rotenone-induced in vitro: Human neuroblastoma SH-SY5Y ↓Mitochondrial dysfunction,
Atg5-mediated autophagy, modulating MMP, ↑Sirt 1,
↓ROS
[57]
LPS-induced in vitro: Microglial BV-2 cells
in vivo: Wistar rats
↑p-GSK-3β, ↑p-Akt, ↑Ser9,
↑Nrf2, ↓NF-κB
[62]
MPTP-induced in vivo: Adult male BALB/c mice ↑Glycolysis, ↑ATP production, ↓motor dysfunction [65]
Rotenone-induced in vivo: Sprague–Dawley rats ↑ATP, ↑SOD, ↑thioredoxin,
[61]
in vitro: Dopaminergic SH-SY5Y cells ↑MAPK, ↓caspase-3, caspase-7, ↓LPO, ↑ERK1/2/5 [67]
TBI/SCI Brain injury in vivo: Wistar
albino male rats
↓MDA, ↑antioxidant potential [93]
SCI in vitro: murine microglia BV2 cells
in vivo: Sprague-Dawley rats
↑Nrf2, ↑HO-1, ↓caspase-3, ↓Bax/Bcl-2 ratio [34]
Oxygen glucose deprivation/re-oxygenation-induced mitochondrial injury in vivo: C57BL/6J mice
in vitro: SMNs
↑Intracellular calcium levels, ↑mPTP, ↓ROS, ↓apoptosis, ↑ATP, ↓Keap1, ↑Nrf2, ↑HO-1, ↑NQO-1 [73]
Neuronal differentiation of BMSCs in vivo: C57BL/6 mice
in vitro: Bone marrow mesenchymal stem cell (BMSC)
↑Nrf2 [74,75]
Secondary damage of TBI in vivo: TBI mouse model
in vitro: Neuro2A cells
↓GPx, ↑MDA, ↓accumulation of free Fe2+ [76]
SCI in vivo: Sprague-Dawley rats
in vitro: Murine microglia BV2 cells
↓TNF-α, ↓IL-1β, ↓NO, ↓iNOS, ↓ IL-6, ↓NF-κB [94]
D-galactose-induced in vivo: Male Kunming mice
in vitro: DPPH
↓TNF-α, ↓IL-1β, ↓IL-6, ↓ caspase-3, ↓Bax/Bcl-2 [30]
Stroke MCAO in vivo: Sprague–Dawley rats ↑Nrf2, ↑HO-1, ↓ROS, ↓p38,
↑Gli1, ↑Ptch1, ↑SOD1
[82,83]
Intracerebral hemorrhage in vivo: Wistar rat ↑Neurological function, ↑NO, ↑SOD, ↑MDA, ↑GSSG, ↑GSH, ↑Nrf2 [95]
MCAO in vivo: Sprague–Dawley rats ↑Bcl-2, ↓IL-1β, ↓TNF-α, ↓ IL-6, ↓Bax, ↓caspases-3/9 [37]
Ischemia–reperfusion injury in vivo: Sprague–Dawley rats ↓CAMs, ↓E-selectin, ↓L-selectin, ↓ICAM-1 [85]
OGD in vitro: Human embryonic kidney cells (HEK-293T)
in vivo: Sprague–Dawley rats
↑MALAT1, ↑CREB, ↑PGC-1α [81]
MCAO in vivo: Sprague–Dawley rats ↓Edema, ↓apoptosis, p53/Notch1 modulation [86]
OGD in vitro: PC12 cell ↓CREB, ↓HIF-1α, ↓p56, ↓Egr1, ↑Ngb, ↓NO [87,88,89]
Hypoxia/ischemia and oxidative stress-induced injury in vitro: N2a cells ↓CREB, ↑BDNF, ↑Shh, ↑Ngb, ↓apoptosis [19,92]

AD: Alzheimer’s disease, Akt: Protein kinase B, Atg5: Autophagy Related 5, ATP: Adenosine triphosphate, Aβ: Amyloid beta, Bcl-2: B-cell lymphoma 2, BDNF: Brain-derived neurotrophic factor, BMSCs: Bone marrow mesenchymal stem cell, CAT: Catalase, Cdk5: Cyclin dependent kinase 5, DPPH: 2,2-diphenyl-1-picrylhydrazyl, Egr1: Early growth response 1, ERK: Extracellular-signal-regulated kinase, GRP78: Glucose-regulated protein, GPx: Glutathione peroxidase, GSH: Glutathione, GSK-3β: Glycogen synthase kinase-3β, GSSG: Glutathione disulfide, HEK-293T: Human embryonic kidney cells, HIBI: Hypoxic-ischemic brain injury, HIF-1α: Hypoxia-inducible factor 1-alpha, HO-1: Heme oxygenase-1, ICAM-1: Intercellular adhesion molecule-1, IL: Interleukin, iNOS: Inducible nitric oxide synthase, LPO: Lipid peroxidation, LPS: Lipopolysaccharides, MALAT1: Metastasis associated lung adenocarcinoma transcript 1, MAPK: Mitogen-activated protein kinase, MCAO: Middle cerebral artery occlusion, MDA: Malondialdehyde, MMP: Matrix metalloproteinase, MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells, Ngb: Neuroglobin, NO: Nitric oxide, Nrf2: Nuclear factor E2-related factor 2, OGD: Oxygen-glucose deprivation, PD: Parkinson’s disease, PTCH1: Protein patched homolog 1, ROS: Reactive oxygen species, SCI: Spinal cord injury, SMNs: spinal motor neurons, SOD: Superoxide dismutase, TBI: Traumatic brain injury, TNF-α: Tumor necrosis factor α.