Estrogen Attenuates Traumatic Brain Injury by Inhibiting the Activation of Microglia and Astrocyte-Mediated Neuroinflammatory Responses

In this study, we constructed an adult male mouse model of TBI and immediately after injury treated the mice with 17 β-estradiol (E2) (100 μg/kg, once every day via intraperitoneal injection) for 3 days. We found that E2 treatment significantly alleviated TBI-induced neurological deficits, neuronal injuries, and brain edema and significantly inhibited Iba1 and GFAP expression, which are markers of microglia an d astrocyte activation, respectively. E2 treatment also significantly inhibited TLR4 and NF-κB protein expression, and significantly reduced the expression of theproinflammatory factors IL-1 β, IL-6, and TNF-α. Moreover, E2 treatment significantly decreased the number of complement C3d/GFAP-positive cells and complement C3d protein expression. Taking these results together, we concluded that E2 treatment dramatically alleviates TBI neuroinflammatory injury by inhibiting TLR4/NF-κB pa thway-mediated microglia and astrocyte activation and neuroinflammation and reducing A1-phenotype neurotoxic astrocyte activation. Our findings indicate that E2 treatment may be a potential therapy strategy for TBI-induced neuroinflammation injury.
Source: Molecular Neurobiology - Category: Neurology Source Type: research