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• W2002257605 abstract "Although 17β-estradiol (E2) is reported to improve the inflammatory response after trauma-hemorrhage (T-H), it remains unknown whether E2 plays any role in the central nervous system after T-H. Microglial cells, resident central macrophages, are thought to play a central role in exacerbating cell-mediated inflammation. We hypothesized that T-H up-regulates microglial cell-mediated inflammatory response in the brain, and E2 produces central anti-inflammatory effects via negative regulation of microglial cells. Male Sprague-Dawley rats were subjected to sham operation (cannulation plus laparotomy) or T-H (midline laparotomy; mean blood pressure, 35 ± 5 mmHg for 90 min followed by resuscitation) and immediately killed after resuscitation. Rats received vehicle or E2 (1 mg/kg body weight i.v.) at the onset of resuscitation. In other experiments, minocycline (40 mg/kg body weight i.p.), microglia inhibitor, was administered 1 h before T-H to prevent inflammatory response in the microglia after T-H. The plasma and hypothalamic tumor necrosis factor (TNF-α) levels were increased, along with the activation of microglial cells in T-H rats compared with shams. Furthermore, T-H increased microglial TNF-α productive capacity in vitro. 17β administration after T-H prevented these inflammatory responses. In rats pretreated with minocycline, decreased microglial TNF-α production and hypothalamic TNF-α levels were observed, but plasma TNF-α levels were not altered after T-H. Thus, T-H induces inflammatory responses even in the hypothalamus, and E2 seems to be a useful adjunct for down-regulating microglial cell-mediated inflammatory response after T-H." @default.
• W2002257605 created "2016-06-24" @default.
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• W2002257605 date "2010-01-01" @default.
• W2002257605 modified "2023-10-12" @default.
• W2002257605 title "MECHANISM OF THE ANTI-INFLAMMATORY EFFECT OF 17β-ESTRADIOL ON BRAIN FOLLOWING TRAUMA-HEMORRHAGE" @default.
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• W2002257605 doi "https://doi.org/10.1097/shk.0b013e3181b0ebcb" @default.
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