Cr (VI) induced oxidative stress and toxicity in cultured cerebellar granule neurons at different stages of development and protective effect of Rosmarinic acid

2014 ◽  
Vol 31 (3) ◽  
pp. 269-277 ◽  
Author(s):  
Abolfazl Dashti ◽  
Maliheh Soodi ◽  
Nahid Amani
Alcohol ◽  
2008 ◽  
Vol 42 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Cynthia J.M. Kane ◽  
Jason Y. Chang ◽  
Paula K. Roberson ◽  
Tarun K. Garg ◽  
Lihong Han

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Susana González-Reyes ◽  
Silvia Guzmán-Beltrán ◽  
Omar Noel Medina-Campos ◽  
José Pedraza-Chaverri

Curcumin is a bifunctional antioxidant derived fromCurcuma longa. This study identifies curcumin as a neuroprotectant against hemin-induced damage in primary cultures of cerebellar granule neurons (CGNs) of rats. Hemin, the oxidized form of heme, is a highly reactive compound that induces cellular injury. Pretreatment of CGNs with 5–30 μM curcumin effectively increased by 2.3–4.9 fold heme oxygenase-1 (HO-1) expression and by 5.6–14.3-fold glutathione (GSH) levels. Moreover, 15 μM curcumin attenuated by 55% the increase in reactive oxygen species (ROS) production, by 94% the reduction of GSH/glutathione disulfide (GSSG) ratio, and by 49% the cell death induced by hemin. The inhibition of heme oxygenase system or GSH synthesis with tin mesoporphyrin and buthionine sulfoximine, respectively, suppressed the protective effect of curcumin against hemin-induced toxicity. These data strongly suggest that HO-1 and GSH play a major role in the protective effect of curcumin. Furthermore, it was found that 24 h of incubation with curcumin increases by 1.4-, 2.3-, and 5.2-fold the activity of glutathione reductase, glutathione S-transferase and superoxide dismutase, respectively. Additionally, it was found that curcumin was capable of inducing nuclear factor (erythroid-derived 2)-like 2 (Nrf2) translocation into the nucleus. These data suggest that the pretreatment with curcumin induces Nrf2 and an antioxidant response that may play an important role in the protective effect of this antioxidant against hemin-induced neuronal death.


2019 ◽  
Vol 8 (3) ◽  
pp. 248-255 ◽  
Author(s):  
Sholeh Akbari ◽  
Maliheh Soodi ◽  
Homa Hajimehdipoor ◽  
Nasim Ataei

Introduction: Alzheimer’s disease (AD) is an age-dependent neurodegenerative disorder and major cause of mortality in the elderly. AD has a complex pathophysiology and needs new multi-targeted compounds to halt the disease progression through several mechanisms. Medicinal plants contain various compounds with heterogeneous pharmacological effects, therefore are a good source. The aim of this study was to evaluate the protective effect of total extracts of Sanguisorba minor and Ferulago angulata on beta-amyloid (Aβ)-induced toxicity in primary neural cell culture.Methods: Cerebellar granule neurons (CGNs) were cultured according to standard protocols. The cultured neurons were incubated with Aβ alone or in combination with different concentrations of extracts for 24 hours. Cell viability was measured by methylthiazolyldiphenyl-tetrazolium (MTT) assay. In addition acetylcholinesterase (AChE) activity and oxidative stress markers were measured after incubation. Also, the effects of different concentrations of the extracts on AChE activity of the cultured neurons were investigated. For measuring the acute toxicity of the extract, LD50 was estimated by limit test.Results: Both extracts could protect CGNs against Aβ-induced cell death. Aβ-induced oxidative stress and increase of AChE activity were ameliorated by both extracts. S. minor extract dose-dependently reduced AChE activity in cultured CGNs. LD50 of both extracts was estimated above 2000 mg/kg and considered as safe.Conclusion: Both studied extracts protected CGNs against Aβ-induced toxicity by ameliorating oxidative stress mechanism. According to these results, these extracts are recommended for further investigation in AD treatment.


Stroke ◽  
2003 ◽  
Vol 34 (7) ◽  
pp. 1796-1802 ◽  
Author(s):  
Yasushi Teshima ◽  
Masaharu Akao ◽  
Ronald A. Li ◽  
Tae H. Chong ◽  
William A. Baumgartner ◽  
...  

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