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Neuroprotective effects of estrogen ...

Min, Irene.

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Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells./
Author:	Min, Irene.
Description:	52 p.
Notes:	Source: Masters Abstracts International, Volume: 48-05, page: .
Contained By:	Masters Abstracts International48-05.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1484789
ISBN:	9781109778526

Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells.
Min, Irene.

Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells. - 52 p.

Source: Masters Abstracts International, Volume: 48-05, page: .

Thesis (M.S.)--Adelphi University, 2010.

Glucose is the primary substrate utilized in the brain as an energy source. Insufficient levels of blood glucose concentration can predispose an individual to potentially debilitating conditions such as hypoglycemia, which, if left untreated, can lead to serious impairment of brain function. Hypoglycemia is the direct result of a homeostatic imbalance within the body. The damaging effects of hypoglycemic stress on hypothalamic neurons have been known to be delayed by estrogen. The present study will focus on demonstrating estrogen's ability to exert a neuroprotective effect against hypoglycemic injury by studying possible pathways taken by estrogen in order to promote cellular survival. The N38 cell line was used and was susceptible to hypoglycemic injury. When compared to cells grown in standard growth media containing glucose, cells grown in glucose free media (hypoglycemic environment) experienced a significant decrease in cell count, indicating cell death. However, it was both qualitatively and quantitatively demonstrated that the addition of varying concentrations of estrogen delayed cell death. By performing the MTT Assay and Cytotoxicity LDH Assay, it was apparent that estrogen was able to delay mitochondrial dysfunction. Furthermore, by performing immunocytochemistry, it is possible that instead of acting through the classical genomic pathway (nuclear receptor), estrogen activates a non-genomic pathway by binding to a receptor on the plasma membrane in the face of hypoglycemia. This possibility was supported by the DNA Microarray results, which indicated that during hypoglycemic injury, the Akt-GSK3b pathway, a non-genomic pathway, is possibly activated. In the presence of estrogen under hypoglycemic stress, Akt is activated which in turn deactivates GSK3b which then possibly inactivates proapoptotic factors such as BAD leading to a decrease in mitchochondrial dysfunction and thus an increase in cellular survival. Thus, the present study demonstrates estrogens ability to exert a neuroprotective effect on neurons during hypoglycemic stress.

ISBN: 9781109778526Subjects--Topical Terms:

1017719
Biology, Molecular.

Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells.
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020 $a 9781109778526
035 $a (UMI)AAI1484789
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100 1 $a Min, Irene. $3 1669156
245 1 0 $a Neuroprotective effects of estrogen against hypoglycemic injury on hypothalamic cells.
300 $a 52 p.
500 $a Source: Masters Abstracts International, Volume: 48-05, page: .
500 $a Adviser: Tandra Chakraborty.
502 $a Thesis (M.S.)--Adelphi University, 2010.
520 $a Glucose is the primary substrate utilized in the brain as an energy source. Insufficient levels of blood glucose concentration can predispose an individual to potentially debilitating conditions such as hypoglycemia, which, if left untreated, can lead to serious impairment of brain function. Hypoglycemia is the direct result of a homeostatic imbalance within the body. The damaging effects of hypoglycemic stress on hypothalamic neurons have been known to be delayed by estrogen. The present study will focus on demonstrating estrogen's ability to exert a neuroprotective effect against hypoglycemic injury by studying possible pathways taken by estrogen in order to promote cellular survival. The N38 cell line was used and was susceptible to hypoglycemic injury. When compared to cells grown in standard growth media containing glucose, cells grown in glucose free media (hypoglycemic environment) experienced a significant decrease in cell count, indicating cell death. However, it was both qualitatively and quantitatively demonstrated that the addition of varying concentrations of estrogen delayed cell death. By performing the MTT Assay and Cytotoxicity LDH Assay, it was apparent that estrogen was able to delay mitochondrial dysfunction. Furthermore, by performing immunocytochemistry, it is possible that instead of acting through the classical genomic pathway (nuclear receptor), estrogen activates a non-genomic pathway by binding to a receptor on the plasma membrane in the face of hypoglycemia. This possibility was supported by the DNA Microarray results, which indicated that during hypoglycemic injury, the Akt-GSK3b pathway, a non-genomic pathway, is possibly activated. In the presence of estrogen under hypoglycemic stress, Akt is activated which in turn deactivates GSK3b which then possibly inactivates proapoptotic factors such as BAD leading to a decrease in mitchochondrial dysfunction and thus an increase in cellular survival. Thus, the present study demonstrates estrogens ability to exert a neuroprotective effect on neurons during hypoglycemic stress.
590 $a School code: 0001.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Physiology. $3 1017816
690 $a 0307
690 $a 0317
690 $a 0719
710 2 $a Adelphi University. $3 1017872
773 0 $t Masters Abstracts International $g 48-05.
790 1 0 $a Chakraborty, Tandra, $e advisor
790 $a 0001
791 $a M.S.
792 $a 2010
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1484789