Rosiridin Attenuates Scopolamine-Induced Cognitive Impairments in Rats via Inhibition of Oxidative and Nitrative Stress Leaded Caspase-3/9 and TNF-α Signaling Pathways

• Published in: Molecules (Basel, Switzerland) Switzerland), 2022-09, Vol.27 (18), p.5888
• Main Authors: Afzal, Muhammad, Alzarea, Sami I, Alharbi, Khalid Saad, Alzarea, Abdulaziz I, Alenezi, Sattam Khulaif, Alshammari, Mohammed Salem, Alquraini, Ali H, Kazmi, Imran
• Format: Article
• Language: English
• Subjects: Acetylcholine; Acetylcholine - pharmacology; Acetylcholinesterase; Acetylcholinesterase - metabolism; Acetyltransferase; Acute toxicity; Alzheimer's disease; Animal cognition; Animals; Antioxidants; Apoptosis; Binding sites; Biocompatibility; Brain research; Burnout; Care and treatment; Caspase 3 - metabolism; Caspase-3; Catalase; Catalase - metabolism; Central nervous system; Choline; choline acetyltransferase; Choline O-acetyltransferase; Choline O-Acetyltransferase - metabolism; Cognition; Cognition disorders; Cognitive ability; Cognitive Dysfunction - chemically induced; Cognitive Dysfunction - drug therapy; Dementia; Disease control; Dosage and administration; Experiments; Gene expression; Glutathione - metabolism; Herbal medicine; Humans; IL-1β; Inflammation; Inhibition (psychology); Interferon; Interferon-gamma - metabolism; Interleukin 6; Interleukin-6 - metabolism; Laboratories; Latency; Maze Learning; Memory; Monoterpenes - pharmacology; Monoterpenoids; Neurodegeneration; neuroprotective; Nitrates - pharmacology; Oxidative Stress; Parameter estimation; Physiology; Rats; rosiridin; Scopolamine; Scopolamine - adverse effects; Signal Transduction; Superoxide dismutase; Superoxide Dismutase - metabolism; Testing; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-α
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules27185888

A monoterpene and bioactive component of the plant ( ), rosiridin has beneficial effects on the human central nervous system and enhances brain function. The goal of this scientific study was to determine if rosiridin might shield rats from neurocognitive problems induced by scopolamine. To track the potential toxicities in rats, the acute toxicity in rats was clarified. Rosiridin at a dose of 10 mg/kg was tested in rats for 14 days. At the conclusion of the investigation, behavioral parameters that were used to identify the rats' cognitive and motor abilities were evaluated. Several biochemical parameters were estimated using the prepared homogenate, including acetylcholine esterase (AChE), choline acetyltransferase (ChAT), radical scavengers produced by the body (Catalase-CAT, superoxide dismutase-SOD, and reduced glutathione-GSH), indicators of oxidative and nitrative burnout, pro-inflammatory (Interleukins- IL-1β, IL-6, interferon gamma IFN-ꝩ, and tumor necrosis factor-TNF-α), and cell apoptosis caspases 3 and 9. 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.