The Soy Isoflavone, Genistein, Protects Human Cortical Neuronal Cells from Oxidative Stress

• Published in: Neurotoxicology (Park Forest South) Vol. 25; no. 5; pp. 885 - 891
• Main Authors: Sonee, Manisha, Sum, Tak, Wang, Chunyang, Mukherjee, Suman K
• Format: Journal Article
• Language: English
• Published: Orlando, FL Elsevier B.V 01.09.2004; Elsevier
• Subjects: Apoptosis; Apoptosis - drug effects; Biological and medical sciences; Cell Death - drug effects; Cell Line; Cerebral Cortex - drug effects; Cerebral Cortex - pathology; Down-Regulation - drug effects; Enzyme-Linked Immunosorbent Assay; Estradiol - pharmacology; Genistein; Genistein - pharmacology; Human cortical neurons; Humans; L-Lactate Dehydrogenase - metabolism; Medical sciences; Necrosis; Neurons - drug effects; Neurons - pathology; Neuroprotective Agents; Oxidative Stress - drug effects; Proto-Oncogene Proteins c-bcl-2 - metabolism; tert-Butylhydroperoxide - toxicity; Tertiary butylhydroperoxide; Toxicology; Genistein; Human cortical neurons; Tertiary butylhydroperoxide; Apoptosis; Necrosis; Human; Oxidative stress; Soybean; Isoflavone derivatives; Phytoestrogen; Prevention; Neuron; Cell death
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2003.11.001

Genistein, a soy isoflavone, has been shown to mimic the pharmacological actions of the endogenous steroid estrogen with which it has structural similarities. There is now evidence that the genistein can prevent disorders-like heart diseases, cancer and diabetes as well. However, very few studies have looked at the effect of genistein on the central nervous system. Published studies also show conflicting conclusions regarding the effects of genistein in the brain. The current study was conducted in the human cortical cell lines HCN1-A and HCN2 in order to determine the neuroprotective efficacy of genistein. It was observed that pre-treatment with 50 or 10 μM genistein was able to protect HCN1-A and HCN2 cells from the cell death induced by 100 μM or 1 mM tertiary butylhydroperoxide ( t-BuOOH; a free radical generating toxin). The morphological disruption caused by t-BuOOH was also prevented by genistein in HCN2 cells. Moreover, genistein was able to prevent the down-regulation of the anti-apoptotic protein bcl-2 that was caused by t-BuOOH treatment. These results indicate that genistein may have neuroprotective effect in cortical cells, which may be mediated by its regulation of the anti-apoptotic protein bcl-2.