Rosiridin Attenuates Scopolamine-Induced Cognitive Impairments in Rats via Inhibition of Oxidative and Nitrative Stress Leaded Caspase-3/9 and TNF-α Signaling Pathways.
Muhammad AfzalSami I AlzareaKhalid Saad AlharbiAbdulaziz I AlzareaSattam Khulaif AleneziMohammed Salem AlshammariAli H AlqurainiImran KazmiPublished in: Molecules (Basel, Switzerland) (2022)
A significant behavioral parameter restoration was seen in the rosiridin-treated group, including reduction in latency time during acquisition and retention trial in the Morris water maze test, and percentage of spontaneous alterations in the y-maze test, when compared to the disease control group that received scopolamine; rosiridin also altered the oxidative stress and neuroinflammatory markers, as well as restoring Ach and ChAT activities and normalizing GSH, SOD, MDA, TNF-α, nitrate, IL-1β, IL-6, IFN-ꝩ, caspases 3 and 9 levels. The results imply that rosiridin limits the effect of scopolamine on rat cognitive function.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- rheumatoid arthritis
- signaling pathway
- high glucose
- cell death
- clinical trial
- nitric oxide
- dna damage
- dendritic cells
- study protocol
- immune response
- phase iii
- ischemia reperfusion injury
- breast cancer cells
- endoplasmic reticulum stress
- stress induced
- drug induced
- epithelial mesenchymal transition
- endothelial cells
- amyotrophic lateral sclerosis
- pi k akt
- newly diagnosed
- heat stress
- heat shock
- placebo controlled