The role of secretory leukoprotease inhibitor(SLPI) in cerebral ischemia

首先，我们研究了星形胶质细胞在低氧状态下的葡萄糖代谢。低氧诱导星形胶质细胞磷酸戊糖途径(PPP)激活。低氧激活PPP伴随着Nrf2移位至胞核，而不伴随Bip在内质网的表达。接下来，我们研究了分泌型白蛋白水解酶抑制剂(SLPI)在缺血再灌注损伤中对细胞损伤的影响。在缺氧缺糖时，SLPI增加了神经元中Alamar Blue的还原，而SLPI不影响星形胶质细胞的活性。星形胶质细胞和神经元在脑缺血中的作用可能不同。

First, we investigated glucose metabolism in astroglia during hypoxia. Hypoxia without glucoprivation induced pentose phosphate pathway(PPP) activation in astroglia. PPP activation by hypoxia was accompanied by Nrf2 translocation to the nucleus but not by Bip expression in the ER. Next, we investigated the effects of secretory leukoprotease inhibitor(SLPI) on the cell damage during ischemic-reperfusion injury. Alamar Blue reduction increased by SLPI during oxygen glucose deprivation in neurons, while SLPI did not affect astroglial cell viability. The effects of SLPI in cerebral ischemia might be different between astrocytes and neurons.