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] |