Changes in the gene expression of estrogen receptors involved in the protective effect of estrogen in rat's trumatic brain injury.

It has been demonstrated that estradiol has neuroprotective effects after traumatic brain injury (TBI) in female rats. Since estrogen receptors have an important role in estradiol effects at the cellular level and the exact mechanism(s) of estradiol-induced neuroprotection has not yet been fully clarified, the present study was designed to determine the changes in the levels of estrogen receptors mRNAs and proteins involved in this phenomenon. All experiments were carried out on female Wistar rats. The brain edema and blood-brain-barrier (BBB) disruption were assessed. The TBI method was diffuse type and induced by the Marmarou method. Semiquantitative RT-PCR and immunoblotting were used to assess ERα and ERβ gene expression. The data showed that the level of brain water content was significantly increased in TBI group. The increased water content was significantly attenuated in estradiol-treated (1mg/kg) TBI rats. Disruption of BBB after TBI was significantly inhibited just by estradiol treatment. Estrogen-treated animals showed a significant increase in ERα mRNA (18%) and protein (35%) levels in the brain tissue. Furthermore, in the brain-injured rats the levels of ERβ mRNA were lower than those in control rats. Following estrogen treatment, the protein levels of ERβ were closed to those in control group. In conclusion, the data demonstrate that estrogen treatment can protect brain against traumatic brain injury. Estrogen treatment increases ER mRNA and protein levels which were coincident with its protective effects. It seems that such phenomenon participates in the induction of neuroprotective effects of estrogen. This article is part of a Special Issue entitled 1618.