Research Reports - Contribution of estrogen receptors alpha and beta in the brain response to traumatic brain injury

J Neurosurg. 2013 Aug;119(2):353-61

Asl SZ, Khaksari M, Khachki AS, Shahrokhi N, Nourizade S

Object Although there is evidence that estradiol has neuroprotective effects
after traumatic brain injury (TBI) in female rats, it is unclear which estrogen
receptor (ER) subtype, ERα or ERβ, mediates this effect. The authors therefore
examined the roles of the different ERs in this effect. Here the authors used the
ERα selective agonist propyl pyrazole triol (PPT) and the ERβ selective agonist
diarylpropionitrile (DPN) alone and in combination in female rats to investigate
this question. Methods Before the ovariectomized animals were injured using the
Marmarou TBI technique, they were randomly divided into the following 9 groups:
control, sham, TBI, vehicle, E1 (physiological dose of 17-β estradiol), E2
(pharmacological dose of 17-β estradiol), PPT, DPN, and PPT+DPN. Levels of
blood-brain barrier (BBB) disruption (5 hours) and water content (24 hours) were
evaluated after TBI. In groups receiving drugs or vehicle, treatment was
administered as a single dose intraperitoneally 30 minutes after induction of
TBI. Results Results showed that brain edema or brain water content after TBI was
lower (p < 0.001) in the E2, PPT, DPN, and PPT+DPN groups than it was in the
vehicle group. After trauma, the Evans blue dye content or BBB permeability was
significantly higher in the TBI and vehicle groups (p < 0.001) than in the E2,
PPT, DPN, and PPT+DPN groups. The inhibitory effects of PPT+DPN on brain water
content, neurological scores, and Evans blue dye content were the highest for all
groups. Although both PPT and DPN increased neurological scores after TBI, PPT
appears to be more effective in increasing neurological scores. Conclusions
Neuroprotective effects of estradiol on brain edema, BBB permeability, and
neurological scores are mediated through both ERα and ERβ. This may suggest a
therapeutic potential in the brain trauma for ER-specific agonists.

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