Table 1.

Effects of resveratrol on glial cell in experimental models of stroke

Resveratrol treatment	Model	Glial cell type	Results	Ref.
100 mg/kg i.p. once per day for 14 days	Intracerebral hemorrhage	Microglia	↓Secondary brain injury ↑Motor abilities ↓Neural damage ↓Activation of microglia	(Cai et al., 2018 ▶)
50 nmol/μL at L4–6 segments of the spinal cord	Spinal cord ischemia/reperfusion	Astrocytes Microglial	↓Inflammation	(Li et al., 2014 ▶)
30 mg/kg i.p. at 24 h after ischemia	Global cerebral ischemic injury	Astrocytes Microglial	↓Cerebral ischemic injury	(Wang et al.,2002 ▶)
25 μmol/L (culture medium)	Rodent astrocyte cultures and an in vivo stroke model	Astrocytes	↑Mitochondrial function	(Narayanan et al., 2015 ▶)
20 mg/Kg i. p.	Hypoxic–ischemic model	Astrocytes	↓Infarct volume ↑Mitochondrial function ↓ROS ↓Neuronal loss	(Arteaga et al., 2015 ▶)
20 mg/kg i. p; 10 min before hypoxia	Hypoxic–ischemic model	Astrocytes Microglial	↓TNF-α, COX2, caspase 3 No differences were observed in SOD2 expression	(Revuelta et al., 2017 ▶)
1, 10mg/kg i.p for 21 days	Forebrain global ischemia	Astrocytes Microglial	↓GLT-1 expression ↑CA1 neuronal protection	(Girbovan and Plamondon, 2015 ▶)
20 mg/kg, 10 min before hypoxia	Hypoxic ischemic	Astrocytes Oligodendrocytes	↑Body and brain weight ↓ROS	(Revuelta et al. 2016 ▶)
30, 60, 90 mg/kg i.p. at 2 and 12 h post-injury 1, 10, 20 µM (culture medium)	Subarachnoid hemorrhage and in vitro experiment in primary cultured cortical neurons	Microglial	↓Inflammation ↓Brain edema ↓Neurobehavioral impairment ↓Apoptosis ↓Neuronal degeneration	(Zhang et al., 2017b ▶)
60 mg/kg i.p., 1 h after SAH	Subarachnoid hemorrhage	Astrocytes Microglial	↓Inflammation ↓Apoptosis	(Zhao et al., 2017 ▶)
1, 2.5, or 5 mg/kg, i.v, 3 or 6 h after MCAO	Middle cerebral artery occlusion model	Microglia	↓IL-1β ↓TNF-α ↓Microglial activation ↓ROS	(Shin et al., 2010 ▶)
60 mg/kg at 2 and 12 h post-injury	Subarachnoid hemorrhage	Microglia	↓Microglia activation ↓Inflammatory cytokines ↓Apoptosis ↓Brain edema ↓Neurological deficit score ↓NF-κB	(Zhang et al., 2016a ▶)
20, 50 mg/kg i.p, daily pre-ischemic injections starting on day 7	Focal cerebral ischemia	Astrocytes Microglia	↓Infarct volume ↑Blood-brain-barrier integrity ↓Bax, caspase-3 ↑Angiogenesis and neurogenesis ↑GDNF and VEGF	(Hermann et al., 2015 ▶)
100 mg/kg, i.p., injected three times at 0 h, 8 h and 18 h after hypoxic-ischemic	Neonatal hypoxic-ischemic	Microglia	↓Inflammation ↓Microglia activation ↓Apoptosis ↓Bax ↓Bcl-2 ↓Caspase3	(Pan et al., 2016 ▶)
30 mg/kg, i.p., every day for 7 days before ischemia	Global ischemia	Astrocytes Microglia	↓Astroglial and microglial activation ↓COX2 and iNOS production ↓Inflammation	(Simão et al., 2012 ▶)
100 mg/kg i.p., injected at 0, 8 and 18 h after cerebral ischemia	Middle cerebral artery occlusion	Microglia	↓MiR-155 expression ↑M2 polarization of microglia ↓Neuroinflammation	(Ma et al., 2019 ▶)
5, 10, 20, 40 mg/ kg, i.p., administered from day 1 after surgery till 27 days	Intracerebral hemorrhage	Microglia	↑Neurological scoring tests ↑Anti-inflammatory and antioxidant factors	(Singh et al., 2017 ▶)
10 mg/kg i.p for 20 days	Ischemia/reperfusion	Microglia	↓Inflammation ↓Ionized calcium binding adaptor molecule 1 ↓Neuronal apoptosis	(Zhao et al., 2019 ▶)

Bax: Bcl-2-associated x protein; Bcl-2: B-cell lymphoma 2; COX2: Cyclooxygenase 2; SOD2: Superoxide dismutase 2; DMSO: Dimethyl sulfoxide; GDNF: Glial cell-derived neurotrophic factor; GLT-1: Glutamate transporter 1; HI: hypoxic-ischemic; i.p: Intraperitoneal; ICH: Intracerebral hemorrhage; IL-1β: Interleukin 1 beta; iNOS: Inducible nitric oxide synthase; MCAO: Middle cerebral artery occlusion; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; ROS: Reactive oxygen species; SAH: Subarachnoid hemorrhage; TNF-α: Tumor necrosis factor alpha; VEGF: Vascular endothelial growth factor.