IGF-II is a pleiotropic hormone widely distributed in the CNS, which
triggers its functions by binding to IGF-IR, InsulinR and IGFII / M6P
(IGF-IIR) receptors. Recently, it has been proposed that the effects of
IGF-II, interacting with IGF-IIR, are relevant not only for metabolism,
growth and development, but also for neurotransmitter release, memory
consolidation and neuroprotection under neurodegenerative processes.
The results of our research group prove that IGF-II exerts metabolic,
antioxidant and neuroprotective effects in aging. In relation to
glucocorticoids, it has been revealed that the exposure of neural cells to
high levels or prolonged incubation periods, produce synaptic alteration,
neurodegeneration and neuronal death. Mechanisms of glucocorticoiddamage
are mediated by oxidative stress induced by an increase in ROS,
mitochondrial damage, decrease in antioxidant defenses, lipid and
protein membrane damage, etc. AIM: To study the antioxidant and
neuroprotective effect of IGF-II in a model of oxidative damage induced
by glucocorticoids in aging. Results:Incubation of cells with CORT triggers oxidative damage, consuming
antioxidant status. This oxidative stress produces damage and
mitochondrial redistribution inducing synaptic changes, as shown the
decrease in synaptophysin and PSD95 levels together with a decrease in
the uptake and release of FM1-43, which may result in
neurodegeneration. Incubation with IGF-II reverses these deleterious
effects. Conclusions: Treatment of cells with IGF-II recovers the
damage produced by CORT, restoring synaptic function and decreasing
neurodegeneration. These outcomes can be attributed to an antioxidant
effect mediated by the interaction of IGF-II with its specific IGF-IIR,
which in turn mediates recovery of the redox balance via inhibition of
ROS production, improvement of mitochondrial membrane potential /
distribution and / or regulation of synaptic proteins.
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