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] |