Neuroprotection of 17β-Estradiol Against D-Glucose Exposure Effect on Tyrosine Hydroxylase Expression and Apoptotic Cells in Zebrafish

Impaired glucose balance affects the regeneration of neurotransmitters in the brain. One of neurotransmitters that is known to have an important role in the brain is dopamine. Dopamine production by dopaminergic (DA) neurons is regulated by the enzyme tyrosine hydroxylase (TH). Previous research has been reported that a decline on TH expression in DA neurons was a result of exposure to excess glucose. One contributing factor is an excess amount of glucose, which interfere homeostasis in the body by producing reactive oxygen species (ROS) more and cause oxidative stress. This condition can cause damage to cells in the brain, including DA neurons, to cell death occurs (apoptosis). The characteristic of neuroprotective owned by the hormone estrogen allegedly able to protect nerve cells from the damaging effects of this. The aim of this study is to explore the involvement of 17β-Estradiol as neuroprotection on the effects of glucose exposure during early development on dopaminergic neurons. This study used zebrafish (Danio rerio) embryos as animal model. They were divided into 4 groups: negative control group, hyperglycemia group, group that was coincubated glucose and estrogen, and the group that only incubated with estrogen alone. Cell death (apoptosis) in the brain was observed using acridine orange staining and TH expression was observed using immunocytochemistry. The results showed that the embryos were exposed to 5% glucose significantly (p less than 0.05) increased the number of apoptotic cells and decreased the expression of TH. While the results of the analysis of embryos in co-incubation group with estrogen showed improvement with decreased apoptotic cells and the increasing expression of TH up to the normal amount. It can be concluded that estrogen shown to have neuroprotective effect in protecting the decreasing TH expression, as the effects of glucose exposure, which could potentially lead to diabetes, by acting as an antioxidant through cellular mechanisms in the central nervous system