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]