Table 3 Impact of resveratrol on the expression of genes in the context of diabetic complications
Type of disease | Dose range | Cell line | Target | Pathway | Function | Refs. |
|---|---|---|---|---|---|---|
In vivo studies | ||||||
Diabetic cardiomyopathy (DCM) | 5–50 mg/kg, 10 μM | Ventricular myocytes | Bax, Bcl-2, Histone H3 | PI3K/AKT/FoxO3a | RVT via the PI3K/AKT/FoxO3a pathway by inhibiting apoptosis could ameliorate cardiac dysfunction in DCM | [36] |
Type 1 diabetes (T1D) | 40 mg/kg | – | GSK-3β, PTEN, Nrf2, NQO-1, HO-1, p62, Caspase-3, LC3II, Keap1 | AKT | RVT by AKT-mediated Nrf2 activation via p62-dependent Keap1 degradation could reduce testicular apoptosis in T1D mice | [41] |
Type 2 diabetes | 100 mg/kg, 0–100 μM | HepG2 | miR-363-3p, FOXO1, G6PC | PI3K/AKT | RVT by upregulating mmu-miR-363-3p via the PI3K/AKT pathway could reverse high-fat diet (HFD)-induced insulin resistance | [37] |
Neuropathic pain | 40 mg/mL | – | SIRT1/PGC1α | PI3K/AKT | RVT via PI3K/AKT and SIRT1/PGC1α pathways could inhibit paclitaxel-induced neuropathic pain | [42] |
Diabetic nephropathy (DN) | 10 mg/kg, 25 μM | Rat Mesangial Cell (RMC) | PAI-1 | AKT/NF-κB p65 | RVT via inhibiting AKT/NF-κB pathway could prevent mesangial cell proliferation and diabetes-induced renal inflammation | [35] |
In vitro studies | ||||||
DN | 10 μM | PC12 | Bim, FoxO3a | PI3K/AKT | RVT via the PI3K/AKT/FoxO3a pathway could attenuate the HG-induced oxidative stress and apoptosis in PC12 cells | [39] |
Diabetes mellitus | 100 μM | NP | Caspase-3, Bcl-2, Bax, p53 | PI3K/AKT | RVT via activating PI3K/AKT pathway could attenuate high glucose-induced NP cell senescence and apoptosis | [38] |