bisabolol has been researched along with Memory-Disorders* in 2 studies
2 other study(ies) available for bisabolol and Memory-Disorders
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(-)-α-bisabolol exerts neuroprotective effects against pentylenetetrazole-induced seizures in rats by targeting inflammation and oxidative stress.
Epilepsy is the most common neurological disorder which is accompanied with behavioral and psychiatric alternations. Current evidences have shown that (-)-α-bisabolol (BSB) possess anti-inflammatory and antioxidative effects in several animal studies. Here, we conducted present study to evaluate its neuroprotective effects against pentylenetetrazole (PTZ)-induced seizures in rats. We used fifty male rats and they were randomly assigned into 5 groups control, BSB100, PTZ, BSB50 + PTZ, BSB100 + PTZ. The animals intraperitoneally received PTZ (45 mg/kg) for ten consecutive days to induce epilepsy model. BSB in doses of 50 and 100 mg/kg was administrated orally one hour before PTZ administration for ten days. The elevated plus maze (EPM) test was carried out to assess anxiety-like behavior. The seizure intensity was evaluated according to modifies Racine's convulsion scale (RCS). Y-maze and passive avoidance were utilized to assess working memory and aversive memory. The expression of pro-inflammatory cytokines and oxidative stress factors were measured using the enzyme-linked immunosorbent assay (ELISA). The neuronal cell loss in the hilar region was assessed using Nissl staining. Results showed that PTZ-treated rats had more seizure intensity, anxiety-like behavior, memory deficits, higher levels of TNF-α, IL-1β, and oxidative markers. Pre-treatment with BSB 100 significantly inhibited seizure intensity, anxiety-like behavior, and memory deficits; reduced levels of TNF-α, IL-1β, and MDA oxidative markers. Collectively, outcome of this work shows that BSB at the dose of 100 mg/kg may exert neuroprotective effects by mitigating seizures, oxidative stress, and neuroinflammation, and ameliorates memory and anxiety disorders in the PTZ-induced seizure rats. Topics: Animals; Anticonvulsants; Disease Models, Animal; Epilepsy; Inflammation; Male; Memory Disorders; Neuroprotective Agents; Oxidative Stress; Pentylenetetrazole; Rats; Rats, Wistar; Seizures; Tumor Necrosis Factor-alpha | 2023 |
(-)-α-bisabolol prevents neuronal damage and memory deficits through reduction of proinflammatory markers induced by permanent focal cerebral ischemia in mice.
The pathophysiology of ischemic stroke involves multiple events such as inflammation and oxidative stress which will lead to neuronal death and cognitive deficits. The (-)-α-bisabolol is a monocyclic sesquiterpene alcohol found in various plants and mainly in Matricaria chamomilla, which exerts antioxidant, anti-inflammatory, and anti-apoptotic activities. The aim of this work was to investigate the neuroprotective effects of (-)-α-bisabolol in mice underwent permanent occlusion of the middle cerebral artery (pMCAO). Animals were treated with (-)-α-bisabolol (50, 100 and 200 mg/kg/day, orally) or vehicle (3% tween 80) one day before and 1 h after pMCAO and the treatment continued once daily for the following five days. The treatment with (-)-α-bisabolol (100 and 200 mg/kg) significantly reduced the infarcted area and neurological deficits caused by pMCAO. (-)-α-bisabolol at the 200 mg/kg dose increased cell viability and decreased neuronal degeneration, as evaluated by cresyl violet and Fluoro-Jade C stainings, respectively. (-)-α-bisabolol also increased the locomotor activity which was reduced by cerebral ischemia and improved pMCAO-induced working, spatial, object recognition, and aversive memories deficits. (-)-α-bisabolol (200 mg/kg) significantly prevented the increase of myeloperoxidase (MPO) activity, TNF-α immunoreactivity in the temporal cortex, and the increase of iNOS both in the temporal cortex and in the striatum. (-)-α-bisabolol treatment also prevented astrogliosis in these areas. These data showed that (-)-α-bisabolol provides neuroprotective action probably due to its anti-inflammatory activity, although other mechanisms cannot be discarded. Topics: Animals; Biomarkers; Cell Death; Infarction, Middle Cerebral Artery; Inflammation; Male; Maze Learning; Memory Disorders; Mice; Monocyclic Sesquiterpenes; Neurons; Neuroprotective Agents; Sesquiterpenes | 2019 |