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Showing 4 results for Amiri
Mohammad Reza Sailani, Zohreh Hojati, Maryam Amiri, Liana Lachinani,
Volume 6, Issue 2 (11-2007)
Abstract
Huntington's disease (HD) is thought to be due to genetically-programmed degeneration of neurons in certain areas of the brain. This degeneration causes uncontrolled movements, loss of intellectual faculties, and emotional disturbances. It is along time since the disease started tormenting human beings, and to date, conventional medications have failed to slow down the progression of HD. Although, the majority of currently-developed drugs may cure the symptoms of HD, they also trigger several side effects such as fatigue, restlessness, or hyper excitability. In the present study, investigation was performed widely on Medieval Persian prescriptions based on medical plants for treatment of the disease. Over 10 valid medical references of medieval Persian texts were screened to have a complete collection. Naturally-occurring substances derived from plants currently have a particular place in drug discovery. In conclusion, the study presents the clinical approaches that practitioners in medieval Persia used to classify, and deal with HD. The accurate observations of medieval Persian physicians provide a precise and comprehensive description of the HD.
Hassan Ahmadvand, Hamze Amiri, Zahra Dehghani Elmi, Shahrokh Bagheri,
Volume 12, Issue 2 (7-2014)
Abstract
Recent investigations have shown that plants have antioxidant properties and could decrease oxidative stress in different human diseases. The present work was identified the chemical composition compounds and evaluated the various antoxidative activities of Ferula-assa-foetida leaves hydroalcoholic extract (FLHE) and Ferula-assa-foetida leaves essential oil (FLEO) . Radical scavenging activity of samples was assessed using Diphenylpicrylhydrazyl (DPPH). Total antioxidant capacity was assessed by methods phosphomolybdat. The amount of total phenol and flavonoid was assessed by Folin-Ciocalteu and Zhishen methods. Also, the components of FLEO were analyzed with gas chromatography/mass spectrometry (GC/MS). In FLHE and FLEO , total antioxidant capacity were 1.55 ± 0.13 and 1.09 ± 0.43 nmol, ascorbic acid equivalents/g, phenol content were 441.37 ± 2.50 and 76.56 ± 9.65 mg of Gallic acid equivalents (GAE)/g, and flavonoid content was 12.53 ± 3.20 and 0.015 ± 0.002 mg of quercetin equivalents/100 g respectively. In the DPPH scavenging assay, the IC 50 values of FLHE, FLEO and Butylated hydroxytoluene (BHT) as reference were 787.13 ± 3.66; 2375.66 ± 5.13 and 3.88 ± 1 ?g/mL respectively . Also GC/MS data and retention indices for reference essential oil leaves samples were used to identify 12 constituents. These compounds made up a total of 85.57% of FLEO : Eremophilene ; ? -cadinene ; Longiborneol; Dehydro aromadendrene; Isoledene; ? -Gurjunene; J-Guaiene. This study showed that ferula-assa-foetida has good antioxidant properties. As it is an easily-accessible source of natural antioxidants such as Eremophilene and ? -cadinene, it may be suitable for use in food and pharmaceutical applications.
Masomeh Emamghoreoshi, Majid Reza Farrokhi, Atena Amiri, Parisa Sarkohi, Mojtaba Keshavarz,
Volume 17, Issue 1 (6-2019)
Abstract
Glycogen synthase kinase (GSK)-3β mediates amyloid-beta (Aβ) and oxidative stress-induced neurotoxicity in neurodegenerative disorders. Natural products with antioxidant activity, such as Sargassum (S.) oligocystum may modulate GSK-3β enzyme and protect against Aβ-induced neurotoxicity. Therefore, we aimed to assess the neuroprotective effects of a methanolic extract of S. oligocystum against Aβ-induced neurotoxicity in the SH-SY5Y cells and the contribution of GSK-3β inhibition to the neuroprotective effects of the S. oligocystum extract. SH-SY5Y neuroblastoma cells were seeded in 96 well plates and incubated with Aβ (20µM) and the methanolic extract of S. oligocystum (40, 50, and 70μg/ml) for 24h. We measured cell viability using the MTT assay. Western blot method was used to measure the expression of the GSK-3β and phosphorylated (p)-GSK-3β protein levels. The data were analyzed using one-way analysis of variance (ANOVA) followed by the LSD test. Amyloid-beta (20µM) reduced neuronal cell viability compared with the control group. Addition of S. oligocystum extract at concentrations of 40, 50 and 70μg/ml decreased the neurotoxic effects of Aβ. The extract of S. oligocystum at a concentration of 70μg/ml also decreased the effects of Aβ on the GSK-3β protein level. The pGSK-3β protein levels in the S. oligocystum groups (40 and 70μg/ml) plus Aβ were lower than the Aβ-treated group. The methanolic extract of S. oligocystum protected SH-SY5Y cells from Aβ-induced neurotoxicity. The attenuation of the GSK-3β protein level may contribute to the neuroprotective effects of S. oligocystum extract.
Mojtaba Keshavarz, Elahe Amirinezhadfard, Mohammad Mehdipour,
Volume 17, Issue 1 (6-2019)
Abstract
Spironolactone has produced beneficial effects in animal models of neurodegenerative disorders. However, the underlying mechanisms of this agent on neurons and glia are mostly unknown. Therefore, we aimed to show the effects of spironolactone and fludrocortisone, a mineralocorticosteroid receptor agonist, on neuronal and glial toxicity induced by N-methyl-D-aspartate (NMDA) activation and chloroquine, an autophagy inhibitor, in the cell culture. We exposed the SHSY5Y neuroblastoma and 1321N1 astrocytoma exposed to NMDA (25µM), or chloroquine (40µM) for 24 and 48h to induce neuronal and glial toxicity. Spironolactone (1, 10, and 20µM) or fludrocortisone (300nM) were also added to the cells for 24 and 48h. Cell survival was measured using the MTT assay. Neurons and astrocytes treated with NMDA and spironolactone (1, 10, and 20µM) for 24 and 48h had lower cell death compared with the NMDA-treated group. Moreover, cells treated with NMDA and fludrocortisone for 24 and 48h had higher viability in comparison to the NMDA-treated group. The neuronal cells treated with chloroquine and spironolactone (10 and 20µM) for 24h had higher cell viability compared with the chloroquine group. Chloroquine plus spironolactone (20µM) treatment for 24 and 48h increased cell viability of astrocytes compared with the chloroquine-treated group. Moreover, the treatment of neurons and astrocytes with chloroquine plus fludrocortisone for 24h decreased cell death. Spironolactone and fludrocortisone protected neurons and astrocytes against NMDA- and chloroquine-induced toxicity. The mechanism of neuronal and glial protective effects of spironolactone possibly related to the inhibition of the mineralocorticosteroids. However, spironolactone might affect other non-mineralocorticoid systems.
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