17β-Estradiol prevents cell death and mitochondrial dysfunction by an estrogen receptor-dependent mechanism in astrocytes after oxygen-glucose deprivation/reperfusion.

摘要: 17β-estradiol (E2) has been shown to protect against ischemic brain injury, yet its targets and the mechanisms are unclear. E2 may exert multiple regulatory actions on astrocytes that greatly contribute ability brain. Mitochondria recognized play central roles in development of injury during ischemia. Increasing evidence indicates mitochondrial critically involved E2-mediated protection. In this study, effect role mitochondria were evaluated primary cultures subjected an ischemia-like condition oxygen-glucose deprivation (OGD)/reperfusion. We showed treatment significantly protects OGD/reperfusion-induced cell death as determined by viability, apoptosis lactate dehydrogenase leakage. The protective effects astrocytic survival blocked estrogen receptor (ER) antagonist (ICI 182,780), mimicked agonist selective for ERα (PPT), but not ER ERβ (DPN). OGD/reperfusion provoked dysfunction manifested increase cellular reactive oxygen species production, loss membrane potential depletion ATP. pretreatment inhibited dysfunction, was also ICI 182,780. Therefore, we concluded provides direct protection from ER-dependent mechanism, highlighting important ERα. Estrogen at early phase injury. However, overall implications ischemia complex sequelae await further exploration.