Table 5.
Impact of resveratrol on the expression of genes in the context of other disorders
| Type of disease | Dose range | Cell line | Target | Pathway | Function | Refs. |
|---|---|---|---|---|---|---|
| In vivo studies | ||||||
| Acute Lung Injury (ALI) | 2.5–10 mg/kg | – | IL-6, KC, MIP-1α, MIP-2, MCP-1, RANTES | PI3K/AKT, ERK | Delivering RVT by polymeric nanocapsules via the ERK/PI3K/AKT pathways could ameliorate LPS-induced ALI | [49] |
| Sepsis | 30 mg/kg | – | MIP-2, IL-18, IL-10, Caspase-3 | PI3K/Nrf2/HO-1 | RVT via inhibiting PI3K/Nrf2/HO-1 pathway could inhibit oxidative stress, inflammation, and cell apoptosis to alleviate ALI in septic rats | [50] |
| Sepsis | 60 mg/kg | – | IL-6, IL-1b, TLR4, Capase-3, Bax, Bcl2, NF-kB | PI3K/AKT/mTOR | RVT via inhibiting the NF-kB and activating the PI3K/AKT/mTOR pathway could protect the myocardium in sepsis | [51] |
| Allergic Diseases | 10 mg/kg, 10–100 μM | BMMCs, FSMCs, PBMCs | IL-6, IL-13, TNF-α, NF-κB, IKKα/β, p65, P-38, Syk, Gab2 | MK2/PI3K/AKT | RVT via the MK2/3–PI3K/AKT axis could inhibit IL-33–mediated mast cell activation | [52] |
| Osteoarthritis (OA) | 45 mg/kg 50 μM | SW1353 | TLR4, MyD88, TRIF, IL-1β, NF-κB p65 | PI3K/AKT | RVT by inhibiting TLR4 via the activation of the PI3K/AKT pathway could inhibit the development of obesity-related OA | [53] |
| Chronic Unpredictable Mild Stress (CUMS) | 40–80 mg/kg | – | TNF-α, IL-6, IL-1β, Bax, Bcl-2 | AKT/GSK-3β | RVT via activating the AKT/GSK-3β pathway could exert a protective effect in CUMS–induced depressive-like behavior | [54] |
| – | 100 mg/kg, 20 μM | 293 T | klf5, c-Myc, Cav-1 | PI3K/PKD1/AKT | RVT via inhibiting the PI3K/PKD1/AKT pathway could activate klf5 phosphorylation and then attenuate the interaction of klf5 with c-Myc | [55] |
| – | 100 mg/kg 40–100 μM | hPASMC | Arginase I, Arginase II, Caspase-3 | PI3K/AKT | RVT via the PI3K/AKT pathway could prevent hypoxia-induced arginase II expression and proliferation of hPASMC | [56] |
| In vitro studies | ||||||
| Thrombosis and atherosclerosis | 1–100 μM | Platelet | PECAM-1, TLR4, STAT3, NF-кB p65, Sirt1 | AKT, AMPK | RVT via STAT3 and AKT pathways could suppress TLR4 activation in oxidized low-density lipoprotein-activated platelets | [48] |
| – | 15 μmol/L | BMSCs, P3 | MyoD1, Myogenin | SIRT1/AKT/FOXO1 | RVT via activating the SIRT1/AKT/FOXO1 pathway could reverse myogenic induction suppression caused by high glucose | [57] |
| – | 20 μM | Chondrocytes | Collagen-II, COX-2, PGE2, JNK, P38 | AKT, ERK, MAPK | RVT via the ERK/p38/AKT pathway could regulate the differentiation and inflammation of chondrocytes | [58] |