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What is the pathway by which estrogen promotes the neuroprotective effect on hypoglycemic injury in hypothalamic cell lines?
Author(s) -
Chakraborty Tandra R.,
Loera Melinda,
Chakraborty Sanjoy
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.823.1
Subject(s) - neuroprotection , hypoglycemia , programmed cell death , apoptosis , estrogen , cell , endocrinology , caspase , glut1 , medicine , arc (geometry) , hypothalamus , diabetes mellitus , pharmacology , chemistry , glucose uptake , biochemistry , insulin , geometry , mathematics
Control of serum glucose level is critically important in reducing the complications of diabetes mellitus. Reports show that recurrent episodes of hypoglycemia can lead to morbidity. In the event of low glucose the regions of the brain like the cortex, hippocampus and hypothalamus become vulnerable to injury. Our preliminary work has shown that estrogen has a neuroprotective effect on hypoglycemic cells. Using parameters like cell count, 3‐(4,5‐Dimethyl‐2‐thiazolyl)‐2,5‐diphrnyltetrazolium bromide (MTT) and Alamar Blue assay, the cells show ∼20% decrease in neuronal cell poliferation when exposed to hypoglycemic shock for 24 hours was observed. However, when beta‐estradiol (100nM) was added to the cells in the absence of glucose under identical conditions there was a ∼10% increase above the control. Neuronal cell death could lead to apoptotic cell death causing activation of caspases. Analyses of caspases‐3 would confer the hypoglycemia‐induced cell death and would be done using immunocytochemical techniques. Further, GLUT1 and ERalpha would be analyzed in the neuronal cells in order to access the signaling pathway and the mechanism of action.