The Role of β-Estradiol in Expression of Protective Neuronal Factors of TGFbeta1, TGFbeta2 and Brain Derived Neurotrophin Factor in Cultured Astrocytes

Author:

Bai Jianbing1,Zhou Shanshan2,Pirouzi Aliyar3,Foruozandeh Hossein3

Affiliation:

1. Department of Neurosurgery, The Affiliated 3201 Hospital of Xi’an Jiaotong University, Hanzhong, Shaanxi, 723000, China

2. Department of Gastrointestinal Surgery, The Affiliated 3201 Hospital of Xi’an Jiaotong University, Hanzhong, Shaanxi, 723000, China

3. Cellular and Molecular Research Center, Gerash University of Medical Sciences, Gerash, 74417-58666, Iran

Abstract

Background: Astrocytes are an important source for the production and release of different cytokines, and their role in the development of neurodegenerative diseases is evident. In the neurodegenerative diseases there are significant changes in these cytokines. For this purpose, the effects of β-estradiol on neuronal protective factors: TGFβ1, TGFβ2 and BDNF were investigated. Methods: In this study, astrocytes from cortex of four newborn rats were isolated and cultivated in cell culture medium. Then their identity confirmed by microscopy and immunocytochemistry. The effect of three different concentrations of β-estradiol (2, 5 and 10 nM) on the expression of selected genes was investigated by Real Time-PCR, also MTT assay was used to evaluate cell viability. Results: In proportion to the increase of β-estradiol concentration, the expression of selective genes changed from 3 to 8 times in comparison to control cells. In addition, by increasing the concentration of β-estradiol, cells exhibited more cellular viability than control cells which was proportional to drug concentration. During neurodegenerative diseases the level of different neuroprotective factors, including the factors selected in this study decreases dramatically. Conclusion: Therefore, increasing the expression of these neuroprotective agents by β-estradiol or other substances may reduce some of the damage associated with astrocytes and prevent disease progression.

Publisher

American Scientific Publishers

Subject

General Materials Science

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