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Propofol is an intravenous anesthetic with neuroprotective effects against cerebral ischemia-reperfusion (I/R) injury. Few studies regarding the neuroprotective and neurobehavioral effects of propofol have been conducted, and the underlying mechanisms are still unclear. Because I/R may result in neuronal apoptosis, the apoptosis regulatory genes B-cell(More)
BACKGROUND Previous studies demonstrate that macrophages synthesis and release catecholamines, which regulate the immune responses in an autocrine manner. These responses are mediated in part by β-adrenoceptors expressed on macrophages. Some β-adrenoceptor antagonists are commonly used in clinical conditions. Here we investigated whether the chronic(More)
Post-operative cerebral edema is a threat for patients performed gliomas resection. Some studies have shown that general anesthesia drugs, such as, propofol had neuroprotective effect. Aquaporin-4 (AQP4) and Aquaporin-9 (AQP9) play an important role in maintaining brain water homeostasis under various conditions. The aim of this study was to compare the(More)
Propofol is a commonly used intravenous anesthetic that has been demonstrated to be neuroprotective against cerebral ischemia-reperfusion (I/R) injury. It remains unclear whether this protective effect has any relationship with the prevention of neuronal mitochondrial deoxyribonucleic acid (mtDNA) deletion. In this study, 81 Wistar rats were randomly(More)
Cerebral ischemia/reperfusion (I/R) injury could cause neural apoptosis that involved the signaling cascades. Cytochrome c release from the mitochondria and the followed activation of caspase 9 and caspase 3 are the important steps. Now, a new mitochondrial protein, apoptosis-inducing factor (AIF), has been shown to have relationship with the(More)
Hypercapnic acidosis may attenuate ventilator-induced lung oxidative stress injury and alveolar cell apoptosis, but the underlying mechanisms are poorly understood. We examined the effects of hypercapnic acidosis on the role of apoptosis signal-regulating kinase 1 (ASK1), which activates the c-Jun N-terminal kinase (JNK) and p38 cascade in both apoptosis(More)
Propofol has been shown to exert neuroprotective effects. Delayed rectifier potassium current (I(K)) was reported to be closely related to neuronal damage. This study was designed to test the effects of propofol on I(K) in rat parietal cortical neurons and the involvement of PKC in this activity. Whole-cell patch-clamp recordings were performed in rat(More)
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