Caffeic Acid Mitigates L-Methionine-Induced Impairment of Hippocampal Neural Stem Cells Through Anti-Apoptotic Signaling in Adult Rats
TL;DR
It is suggested that CA protects against L-met-induced hippocampal neurotoxicity by preserving neurogenesis-related protein expression, attenuating apoptosis-related protein alterations, and maintaining structural integrity.
Abstract
Simple Summary This study evaluated the neuroprotective efficacy of caffeic acid (CA) against chronic L-methionine (L-met)-induced hyperhomocysteinemia and hippocampal neurotoxicity in rats. Twenty-four male Sprague-Dawley rats (n = 6/group) were orally administered vehicle, L-met (1.7 g/kg), CA (40 mg/kg), or CA + L-met for 28 consecutive days. The findings demonstrate that CA administration was associated with preserved hippocampal architecture, characterized by an absence of tissue atrophy and maintenance of the anatomical volumes of both the dentate gyrus and the granule cell layer. Immunofluorescence and molecular analyses demonstrated that CA counteracted L-met-induced neurotoxicity by preventing the depletion of nestin-positive cells and attenuating the downregulation of nestin and Notch-1, key proteins involved in neurogenesis. Furthermore, CA modulated apoptosis-related protein expression by downregulating the pro-apoptotic factors Bax and Caspase-3 and upregulating the anti-apoptotic protein Bcl-2. These findings suggest that CA protects against L-met-induced hippocampal neurotoxicity by preserving neurogenesis-related protein expression, attenuating apoptosis-related protein alterations, and maintaining structural integrity.