Silibinin reduces Alzheimer's neuroinflammationSilibinin ameliorates STING-mediated neuroinflammation via downregulation of ferroptotic damage in a sporadic Alzheimer's disease model.
We explored how silibinin, derived from Silybum marianum, may help combat Alzheimer's disease, particularly the sporadic form that affects most patients. Using a model involving murine hippocampal neurons and rats, we found that silibinin improves cell survival and reduces cognitive decline linked to Alzheimer's.
Those treated with silibinin displayed a notable decrease in neuroinflammation and oxidative stress—two key contributors to Alzheimer’s. It achieves this by regulating proteins involved in cell death. However, it remains essential to continue research to fully understand its benefits and mechanisms before considering practical applications.
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Silibinin shows potential neuroprotectionInhibition of GluN2B pathway is involved in the neuroprotective effect of silibinin on streptozotocin-induced Alzheimer's disease models.
We investigated how silibinin, a compound from Silybum marianum, influences Alzheimer’s disease by targeting N-methyl-D-aspartate receptors (NMDARs). Through various tests on rat models and neurons, we found that silibinin can protect against cell damage caused by streptozotocin (STZ), while specifically inhibiting the GluN2B subunit of NMDARs. This inhibition may help improve learning and memory by positively affecting signaling pathways related to brain function, showcasing silibinin's potential in Alzheimer’s treatment.
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Silybin targets oxidative stress in ADActivation of NRF2/ARE by isosilybin alleviates Aβ25-35-induced oxidative stress injury in HT-22 cells.
We observed that isosilybin, a compound from Silybum marianum, could help reduce oxidative stress linked to Alzheimer's disease. In our study, isosilybin significantly decreased harmful reactive oxygen species and other markers of cell damage in HT-22 hippocampal cells.
It also boosted the production of critical antioxidant proteins through the activation of NRF2/ARE signaling pathways. While the results are promising, it is important to note that the study mainly focused on cellular models, and further in vivo research is needed to confirm these findings in actual Alzheimer’s patients.
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Silibinin counters Alzheimer’s memory lossSilibinin prevents amyloid beta peptide-induced memory impairment and oxidative stress in mice.
We examined the effects of silibinin, a component of the milk thistle plant, on memory impairment linked to amyloid beta-induced oxidative stress in mice. After administering silibinin alongside amyloid beta, we observed promising results; silibinin appeared to prevent memory loss and reduced oxidative damage in the mice's brains.
Our findings suggest that silibinin could be a beneficial treatment for protecting against cognitive decline in Alzheimer's disease. This could open new pathways in the search for effective therapies.
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Silibinin shows promise for cognitionSilibinin Ameliorates Formaldehyde-Induced Cognitive Impairment by Inhibiting Oxidative Stress.
We explored the effects of silibinin, a compound from the milk thistle plant, on cognitive impairment related to Alzheimer's disease. By using a mouse model injected with formaldehyde, we administered silibinin orally for three weeks. The results indicated that silibinin significantly improved memory performance in various cognitive tests, suggesting its ability to reduce cognitive deficits.
While we found promising evidence of its antioxidative effects and potential in enhancing certain signaling pathways, the exact mechanisms remain unclear. Overall, silibinin holds potential as a candidate for improving cognitive health related to Alzheimer’s.
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