ArticleMolecular neurobiology2026
Silibinin Alleviates Cognitive Dysfunction, Biochemical Alterations, and Hippocampal Structural Changes Induced by 5 days of Sleep Deprivation with or Without a Subsequent 24-H Recovery in Rats.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sleep deprivation (SD) impairs cognitive function through oxidative stress, neuroinflammation, and neuroendocrine dysregulation, whereas recovery sleep may not fully reverse these alterations. Silibinin possesses antioxidant, anti-inflammatory, and neuroprotective properties; however, its potential to facilitate recovery following prolonged SD remains unclear. This study investigated the effects of silibinin on cognitive dysfunction and hippocampal alterations induced by 5 days of SD, with or without a subsequent 24-h recovery period, in rats. Forty-eight adult male rats were allocated to control (n = 16), SD (n = 8), SD + recovery (n = 8), SD + silibinin (n = 8), and SD + silibinin + recovery (n = 8) groups. Cognitive performance was assessed using the Open Field Test, Morris Water Maze, and Y-Maze. Serum oxidative stress (MDA and SOD), inflammatory (TNF-α and IL-6), and hormonal biomarkers were evaluated. Hippocampal BDNF and CaMKII levels, histopathological changes, and the immunohistochemical expression of PCNA, synaptophysin, and GFAP were also assessed. SD significantly impaired cognitive performance (P < 0.05), increased oxidative stress and inflammatory cytokines (P < 0.01), altered stress-related hormones (P < 0.05), decreased hippocampal BDNF and CaMKII levels (P < 0.001) and induced marked histopathological and immunohistochemical changes. A 24-h recovery period partially ameliorated these alterations. Silibinin treatment significantly attenuated the SD-induced behavioral, biochemical, hormonal, histopathological, and immunohistochemical alterations (P < 0.05), with further improvement following recovery sleep (P < 0.05), restoring most parameters to levels comparable to those of the control group. These findings suggest that silibinin protects against SD-induced cognitive dysfunction and hippocampal injury by attenuating oxidative stress, neuroinflammation, and neuroendocrine disturbances while enhancing recovery during subsequent recovery sleep.
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