Estrogen receptor agonists induce anti‑edema effects by altering α and β estrogen receptor gene expression.

The present study aimed to examine whether the attenuation of estrogen receptor expression is prevented by propyl pyrazole triol (PPT), an agonist for estrogen receptor α (ERα) or and diarypropiolnitrile (DPN), an agonist for estrogen receptor β (ERβ) after traumatic brain injury (TBI). The tests performed on ovariectomized female Wistar rats included sham group, vehicle group, and treated groups: PPT, DPN, and PPT+DPN 30 minutes after TBI. Blood‑brain barrier (BBB) disruption and brain water content were estimated. RT‑PCR and\r\nwestern blotting were utilized to evaluate ESR1 and ESR2 gene and protein expression. The data indicated that PPT, DPN, and PPT+DPN attenuated TBI‑induced brain edema. Also, BBB disruption after TBI was prevented in PPT, DPN, and PPT+DPN‑treated TBI animals. Estrogen agonist‑treated animals showed a significant elevation in Esr1 mRNA and protein expression levels in the brain tissue of TBI rats. In addition, the data indicated a significant elevation of Esr2 mRNA and protein expression levels in the brain tissue of estrogen agonist‑treated TBI rats. The data shows that both ESR1 and ESR2 agonists can enhance ER mRNA and protein levels in TBI animals' brain. It appears that this effect contributes to the neuroprotective function of ER agonists.