Evidence to implicate early modulation of interleukin-1beta expression in the neuroprotection afforded by 17beta-estradiol in male rats undergone transient middle cerebral artery occlusion.

摘要: Neuroprotection exerted by 17β‐estradiol (17β‐E 2 ) has been widely investigated in animal models of acute cerebral ischemia. Estrogens interact with intracellular receptors (ERα and ERβ) to modulate the transcription target genes, including those implicated neuronal survival. may also occur via interaction ER‐like membrane mediating rapid, non‐genomic, actions or receptor‐independent mechanisms. There is evidence that blockade inflammatory factors represent an important mechanism involved estrogenic neuroprotection. Here we investigate whether reduced brain damage pharmacological treatment 17β‐E male rats subjected transient (2 h) middle artery occlusion (tMCAo) involves modulation interleukin‐1β (IL‐1β), a proinflammatory cytokine strongly pathophysiology ischemic stroke. Administration (0.2 mg/kg, i.p., 1 h before tMCAo) results significant reduction infarct volume, this reverted ER antagonist ICI 182,780 (0.25 mg/kg, i.p.) administered . Two hours MCAo followed 2‐h reperfusion significant, threefold increase IL‐1β levels cortical tissue ipsilateral damage. Interestingly, pretreatment neuroprotective dose attenuates elevation appears through activation. In addition, neuroprotection accompanied cytochrome c translocation both striatum cortex as revealed Western blotting 3 h after reperfusion. conclusion, report original observation rat model focal ischemia cytosol early production.