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. 2022 Sep 30;22:298. doi: 10.1186/s12935-022-02719-3

Table 2.

Impact of resveratrol on the expression of genes in the context of CNS disorders

Type of disease Dose range Cell line Target Pathway Function Refs.
In vivo studies
Subarachnoid Hemorrhage (SAH) 60 mg/kg Beclin-1, LC3-II, Bcl-2, p62, Caspase-3/9 AKT /mTOR RVT via downregulating AKT/mTOR pathway could promote the autophagy process in SAH model rats [19]
Cerebral Ischemia Injury (CII) 30 mg/kg BcL-2, Bax, Caspase-3 JAK2/STAT3, PI3K/AKT/mTOR RVT via activating JAK2/STAT3/PI3K/AKT/mTOR pathway could provide neuroprotection against cerebral I/R injury [20]
CII 100 mg/kg IL-1β, TNFα, COX2 PI3K/AKT RVT via activating PI3K/AKT pathway could attenuate brain damage in permanent focal cerebral ischemia [21]
CII 30 mg/kg AKT/GSK-3β RVT via regulating the AKT/GSK-3β pathway could improve neuronal damage against MCAO-induced CII [24]
CII 20 mg/kg GSK-3β, DJ-1, PTEN, Nrf-2, Bax, Caspase-3, Bcl-2 PI3K/AKT, RVT via reducing of DJ-1 expression and activating of PI3K/AKT/GSK-3β pathway could contribute to post I/R cerebral damage [25]
Chronic cerebral hypoperfusion (CCH) 50 mg/kg Caspase-3, Bcl-2, Bax, LC3B, 4E-BP1, Beclin-1, S6K1 PI3K/AKT/mTOR RVT via the AKT/mTOR pathway could Improve cognitive dysfunction in rats with CCH [26]
Alzheimer’s Disease (AD) 0–40 μM PC12 HO1 PI3K/AKT/Nrf2 RVT by upregulating heme oxygenase-1 (HO-1) via the PI3K/AKT/Nrf2 axis could attenuate the cytotoxicity induced by amyloid-β1–42 in PC12 cells [22]
AD 300 mg/kg PP2A, GSK-3β, Tau, Caspase-3, Bcl2, Bax PI3K/AKT, AMPK RVT via activating PP2A and PI3K/AKT induced-inhibition of GSK-3β could inhibit Tau phosphorylation in rat brain [23]
Parkinson's Disease (PD) 15–30 mg/kg Bax, Bcl-2, Caspase-3, PDK1 PI3K/AKT RVT via activating the PI3K/AKT pathway could protect dopaminergic neurons from 6-hydroxy dopamine (6-OHDA)-induced apoptosis [27]
Spinal Cord Injury (SCI) 100 mg/kg, 40 μM Primary microglia, neurons Beclin-1, Caspase-3, LC3B PI3K RVT-primed exosomes via the PI3K pathway could promote the recovery of motor function in SCI rats [28]
In vitro studies
Intervertebral Disc Degeneration (IVDD) 200 mM NPCs Caspase-3, NF-κB, GSK-3β PI3K/AKT/mTOR RVT and 17β-estradiol via The PI3K/AKT/GSK-3β and PI3K/AKT/mTOR pathways could prevent IL-1β induced apoptosis in the human nucleus pulposus [29]
IVDD 10–200 μM NPCs Caspase-3, MMP-3, MMP-13, COL2a-1, Aggrecan PI3K/AKT RVT and 17β-estradiol via the PI3K/AKT/caspase-3 pathway could play a role in apoptosis induced by interleukin-1β in rat nucleus pulposus cells [30]
IVDD 50–100 μM NP GAPDH, SOX9, Aggrecan, Collagen II PI3K/AKT RVT via activating the PI3K/AKT pathway could increase nucleus pulposus matrix synthesis [31]
IVDD 50 μM NP Aggrecan, Collagen II, Beclin-1, LC3 PI3K/AKT RVT via the PI3K/AKT pathway by activating autophagy could enhance matrix biosynthesis of nucleus pulposus cells [32]