17beta-estradiol suppresses hydrogen peroxide-induced nuclear factor kappa B activation in HT22 cells. Pil J Kim

ISBN: 9781109019391

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NOOKstudy eTextbook

78 pages


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17beta-estradiol suppresses hydrogen peroxide-induced nuclear factor kappa B activation in HT22 cells.  by  Pil J Kim

17beta-estradiol suppresses hydrogen peroxide-induced nuclear factor kappa B activation in HT22 cells. by Pil J Kim
| NOOKstudy eTextbook | PDF, EPUB, FB2, DjVu, AUDIO, mp3, RTF | 78 pages | ISBN: 9781109019391 | 5.50 Mb

Reactive oxygen species (ROS) are natural byproducts of normal cellular reactions. They are oxygen ions, free (non)radicals, and peroxides that are highly reactive with normal macromolecules, such as lipids, DNA, and proteins. Cells are normally ableMoreReactive oxygen species (ROS) are natural byproducts of normal cellular reactions. They are oxygen ions, free (non)radicals, and peroxides that are highly reactive with normal macromolecules, such as lipids, DNA, and proteins. Cells are normally able to defend against the damages of ROS via enzymes that neutralize them into water.

However, when cells are not able to cope with the accumulation of ROS, disruptions in signaling pathways and gene transcription will occur, which will ultimately lead to cell death. It is now widely accepted that increased oxidative stress-induced damage in the brain is a major cause of neurodegenerative diseases, such as Alzheimers disease (AD). Nuclear factor kappaappa-B (NFkappaB) is not only a ubiquitously expressed transcription factor but also a signaling protein that is activated by ROS-induced oxidative stress. Our laboratory has demonstrated the neuroprotective effects of 17beta-estradiol (E2) are elicited via an anti-oxidant effect.

The purpose of this project was to determine the role of NFkappaB activation in E2-mediated neuroprotection against hydrogen peroxide (H2O 2)-induced oxidative stress. HT-22, a murine immortalized hippocampal neuronal cell line, was utilized to determine whether NFkappaB is activated by hydrogen peroxide-induced oxidative stress and whether E2 suppresses H 2O2-induced NFkappaB activation. We observed that H 2O2 activated NFkappaB by phosphorylation of IkappaBalpha (pIkappaBalpha), one of the NFkappaB inhibitor proteins, reduction of total IkappaBalpha, and induction of NFkappaB (p65) nuclear translocation.

In contrast, E2 suppressed H2O2-induced NFkappaB activation by dramatic reducing pIkappaBalpha, increasing total IkappaBalpha, and inhibiting p65 nuclear translocation. Our results show that one of the mechanisms by which estrogens are neuroprotective against oxidative stress is through the attenuation of H2O2-induced NFkappaB activation.



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