In vivo studies |
Intestinal Injury |
20 mg/kg |
– |
TNF-α, NF-κB, IL-1β |
PI3K/AKT/mTOR |
RVT via modulating PI3K/AKT/mTOR pathway could reduce intestinal inflammation in irradiated rats |
[43] |
Liver Fibrosis (LF) |
40–200 mg/kg, 10–50 mg/mL |
HSC-T6 |
miR-20a, α-SMA, TIMP-1, TGF-β1, LC3-II, LC3-I, Beclin1, Atg7 |
PTEN/PI3K/AKT |
RVT via the miR-20a-mediated activation of the PTEN/PI3K/AKT pathway can inhibit LF |
[46] |
LF |
20–50 mg/kg, 0–125 μg/mL |
LX-2 |
α-SMA, Collagen-I, IκB-α, P65 |
AKT, NF-κB |
RVT via the AKT/NF-κB pathways could attenuate the progression of LF |
[47] |
In vitro studies |
Intestinal Damage |
0–50 μM |
IPEC-J2, 293 T |
Claudin-1, Occludin, ZO-1, Keap1, NFE2L2, SOD-1, HO-1, CAT, GSX-1, Nrf2 |
PI3K/AKT |
RVT via the PI3K/AKT-mediated Nrf2 pathway could protect IPEC-J2 cells against oxidative stress |
[44] |
Hepatic Fibrosis |
3.125, 6.25, 12.5 μM |
T-HSC/Cl-6 |
Collagen-I, α-SMA, TLR4, M8, LXR-α, LXR-β |
PI3K/AKT, NF-κB |
RVT via modulating NF-κB and the PI3K/AKT pathway could regulate activated hepatic stellate cells (HSCs) |
[45] |