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Objective: severe liver dysfunction or obstacles in hepatic encephalopathy system due to metabolic disorders as the main feature of the central nervous system dysfunction syndrome. In addition to liver transplantation, there is no effective treatment. Cerebral edema is an important pathological changes in hepatic encephalopathy, the most obvious of which astrocytes edema. Ammonia poisoning is still the central position of the pathogenesis of HE, but its cause astrocytes edema mechanism is not yet fully understood, studies have shown that aquaporin-4 involved in ammonia resulting astrocyte edema. The study showed that propofol via activation of PKC phosphorylation of substrate proteins on ischemia-reperfusion myocardial damage caused neuronal damage and brain edema has a protective effect. To investigate the protective effect of propofol on hepatic encephalopathy, cerebral edema, this study was to establish in vitro model of hepatic encephalopathy by ammonium chloride treatment of primary cultured astrocytes, AQP-4 expression detected at different time points to observe the effect of propofol ammonium chloride treatment astrocyte morphology, cell activity and expression of AQP-4 to explore propofol protective effect of hepatic encephalopathy, cerebral edema and possible mechanisms. Methods: Sprague-Dawley rat cerebral cortex remove students 2-3 days isolated and cultured astrocytes. Primary cultured astrocytes were randomly divided into six groups, respectively, for the control group (normal group), ammonium chloride 6h, 12h, 24h, 48h (NH 4 Cl group) 0.1% dimethyl sulfoxide pretreatment group (DMSO group), PKC agonist TPA pretreatment group (TPA), propofol group (Pro group) and propofol PKC antagonist Ro31-8220 common pre- treatment group (PR group). Purity identification of astrocytes immunofluorescence, Western-blot assay AQP-4 expression in astrocytes, assessed by MTT assay cell activity, optical microscope to observe the morphological changes of astrocytes. Results: 1) compared with the control group, ammonium chloride treatment after 12 h of astrocytes AQP-4 expression was significantly increased (P lt; 0.05), peaked at 24 h to 48 h began to decline. 2) ammonium chloride processing astrocyte activity decreased significantly compared with the control group (P lt; 0.05). 3) NH 4 Cl group, propofol significantly reduce ammonium chloride treated astrocytes AQP-4 upregulation (P lt; 0.05), to reduce cellular edema, suppression The decline in cell activity (P lt; 0.05). 4) of ammonium chloride processing astrocytes fine after PKC agonist TPA pretreatment, compared with NH 4 CL group, AQP-4 expression was significantly lowered (P lt; 0.05), cell activity increased (P lt; 0.05), cell edema. 5) the ammonium chloride processing astrocytes pretreated PKC antagonist Ro31-8220 with propofol, AQP-4 expression was reversible raised, compared with the Pro group, the difference was statistically significant (P lt; 0.05), cell edema. AQP-4 expression in astrocytes Conclusion: ammonium chloride treatment upregulated cells decreased cell edema, and AQP-4 upregulation propofol ammonium chloride pretreatment inhibits astrocyte alleviate cell edema. This effect of propofol in part through activation of the PKC pathway.
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