Neuroprotective Effects of Co UltraPEALut on Secondary Inflammatory Process and Autophagy Involved in Traumatic Brain Injury.
Traumatic brain injury (TBI) initiates a neuroinflammatory cascade that contributes to neuronal damage and behavioral impairment. In the present study, we performed a widely used model of TBI to determine the neuroprotective propriety of palmitoylethanolamide (PEA) and the antioxidant effect of a flavonoid luteolin (Lut) given as a co ultramicronized compound Co ultraPEALut. We demonstrated that the treatment with Co ultraPEALut resulted in a significant improvement of motor and cognitive recovery after controlled cortical impact, as well as markedly reducing lesion volumes. Moreover, our results revealed the ability of Co ultraPEALut to reduce brain trauma through modulation of nuclear factor kB activation. In addition, treatment with Co ultraPEALut significantly enhanced the post TBI expression of the neuroprotective neurotrophins glial cell line derived neurotrophic factor compared with vehicle. Co ultraPEALut at the dose of 1 mg/kg also modulated apoptosis, the release of cytokine and reactive oxygen species, the activation of chymase, tryptase, and nitrotyrosine, and inhibited autophagy. Thus, our data demonstrated that Co ultraPEALut at a lower dose compared with PEA alone can exert neuroprotective effects and the combination of both could improve their ability to counteract the neurodegeneration and neuroinflammation induced by TBI.
Journal of neurotrauma