INVOLVEMENT OF PKCα AND ERK1/2 SIGNALING PATHWAYS IN EGCG'S PROTECTION AGAINST STRESS-INDUCED NEURAL INJURIES IN WISTAR RATS

Stress-induced neural injuries are closely linked to the pathogenesis of various neuropsychiatric disorders and psychosomatic diseases. We and others have previously demonstrated certain protective effects of epigallocatechin-3-gallate (EGCG) in stress-induced cerebral impairments, but the underlying protective mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of PKC alpha and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways in EGCG-mediated protection against restraint stress-induced neural injuries in rats. In both open-field and step-through behavioral tests, the restraint stress-induced neuronal impairments were significantly ameliorated by administration of EGCG or green tea polyphenols (GTPs), which was associated with a partial restoration of normal plasma glucocorticoid, dopamine and serotonin levels. Furthermore, the stress-induced decrease of PKCa and ERK1/2 expression and phosphorylation was significantly attenuated by EGCG and to a less extent by GTP administration. Additionally, EGCG supplementation restored the production of adenosine triphosphate (ATP) and the expression of a key regulator of cellular energy metabolism, the peroxisome proliferators-activated receptor-c coactivator-1 alpha (PGC-1 alpha), in stressed animals. In conclusion, PKC alpha and ERK1/2 signaling pathways as well as PGC-1 alpha-mediated ATP production might be involved in EGCG-mediated protection against stress-induced neural injuries. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.