IGF-1 regulation of oxidative stress in neuroinflammation

ReferenceAuthor (publication year)Neuroinflammatory modelIGF-1 modelOxidative stress markersEffects
[88]Hayes et al., 2021Stroke
E17-19 rat neuronal, astrocytes, and endothelial cell cultures
Glutamate-induced toxicity
Exogenous IGF-1
IGF-1R inhibition with PPP
Dichlorodihydrofluorescein diacetate (DCFDA)IGF-1 can protect neurons from glutamate.
Inhibition of IGF-1R impairs the neuroprotective capabilities of astrocytes.
Inhibition of IGF-1R significantly increases ROS production in both astrocytes and endothelial cells.
[89]Genis et al., 2014Postnatal rats and mice for in vitro cultures (P0–3 days for astrocytes and P7 for neurons) and 3-month-old mice for in vivo experimentsPhysiological IGF-1 measures
IGF-1 deficiency and blockade
H2O2IGF-1 signaling participates in astrocyte neuroprotection against oxidative injury.
IGF-1 decreases the pro-oxidant protein thioredoxin-interacting protein 1 and normalizes the levels of reactive oxygen species.
[90]Grinberg et al., 2013Rat hippocampal slice cultures
Spreading depression
IGF-1 mediumsCellRoxIGF-1 mitigated microglial but not astrocytic oxidative stress from SD.
[91]Tien et al., 2017Intracerebral injection of LPS to 5-day-old Sprague-Dawley rat pupsIntranasal administration of IGF-1COX-2 expressionThe protective effects of IGF-1 are associated with the decrease in microglia activation and reduction of neuronal oxidative stress by suppressing neuronal COX-2 expression in the rat SN, VTA, OB, and LC.
[92]Bake et al., 2014Stroke
Middle-aged female Sprague Dawley rats
Intracerebroventricular infusion of IGF-1 (human recombinant)Levels of thiobarbituric reactive species (TBARS)IGF-1 reduces infarct volume in the acute phase of ischemia-reperfusion injury.
IGF-1 did not attenuate TBAR levels in ischemic tissue.
IGF-1 mediated regulation of inflammatory cytokines in the postischemic brain.
[93]Montivero et al., 2021Traumatic brain injury
Male Wistar rats
Adenoviral IGF-1 gene therapyProtein (AOPP) and lipids (MDA) peroxidationLocally administered IGF-1 gene therapy a few minutes after TBI, significantly reduces recognized oxidative stress markers, such as the protein and lipid (AOPP and MDA concentrations respectively) peroxidation increments observed at 24 h and impairs its long-term maintenance, also by reducing their levels 7 days after TBI.