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Endoplasmic Reticulum Stress is Involved in the Neuroprotective Effect of Propofol.
In this study, we found that propofol up-regulated BiP and attenuated tunicamycin-induced neural cell death. Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP). We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. However, pretreatment with propofol attenuated the levels of phosphorylated protein kinase receptor-like ER kinase, phosphorylated elF2α, ATF4, and caspase-3, but failed to affect the increase of cleaved ATF6 and XBP1s, induced by tunicamyci...
Source: Neurochemical Research - June 25, 2014 Category: Neuroscience Authors: Wang L, Tang W, Jiang T, Lu P, Li Y, Sun A, Shen Y, Chen Y, Wang H, Zong Z, Wang Y, Chen L, Shen Y Tags: Neurochem Res Source Type: research