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AIM: To observe and compare the clinical efficacy and safety of remimazolam and propofol alone and in combination in endoscopic retrograde cholangiopancreatography (ERCP) anesthesia. METHODS: A total of 120 patients undergoing elective ERCP were divided into the propofol group (P group), the remimazolam group (R group), and the remimazolam combined with propofol group (RP group) according to a random number table, with 40 patients in each group, and the three groups completed anesthesia according to the designated drug regimen (propofol in group P; remimazolam in group R; and remimazolam combined with propofol in group RP). General information, operation time and awakening time of the patients in the three groups were compared, as well as oxygen saturation (SpO
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BACKGROUND:Cdh1 has been shown to express in rat hippocampus and cortex in a large number. Moreover, in vitro test demonstrated that Cdh1 expression was higher in neurons than in neural stem cel s, which possibly associated with the differentiation of neural stem cel s into neurons. However, the effects of anaphase promoting complex Cdh1 on ischemic neuronal damage remain unclear. OBJECTIVE:To investigate the expression of Cdh1 and its downstream substrate in primary cultured neurons with oxygen-glucose deprivation. METHODS:Primary neurons from cortex of postnatal 24-hour rat pups were cultured in vitro, and identified by immunofluorescence staining. The oxygen-and glucose-deprived models were established by three gas incubator fil ed with nitrogen in sugar-free Earle’s solution. After 1 hour of hypoxia, reoxygenation was conducted. Real-time fluorescent quantitative PCR was used to detect the mRNA expression of Cdh1 and its downstream substrates Skp2, Cyclin B1 before hypoxia, 6 hours, 1, 3, 7 days after oxygen glucose deprivation. RESULTS AND CONCLUSION:After oxygen glucose deprivation, the expression of Cdh1 and Cyclin B1 in primary neurons was increased (P<0.05), while Skp2 expression was decreased (P<0.05). Above data indicated that Cdh1 expression in neurons increased after oxygen-glucose deprivation. It may degrade Skp2 and participate in hypoxic neuronal apoptosis by ubiquitination.
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@#ObjectiveTo investigate the expression of APC-Cdh1 protein after cerebral ischemia-reperfusion injury.Methods60 male Sprague-Dawley rats were randomly divided into Sham-operated group(SH) and ischemia-reperfusion group(IR). The rats of ischemia-reperfusion groups were induced by four-vessel occlusion (4-VO). At different times after injury, the expression of APC-Cdh1 of rat hippocampus was observed by Western blotting and immunohistochemistry.ResultsCompared with sham-operated group, the expression of Cdh1 protein significantly decreased 1 day and increased obviously 3 days, but decreased again 7 days after injury in ischemia-reperfusion group. The immuno-staining showed that APC-Cdh1 was highly cerebral cortex and hippocampus in ischemia-reperfusion group. ConclusionAPC-Cdh1 may be involved in the central nervous system injury.
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Objective To investigate the role of NF-κB in apoptosis of immortalized neural progenitor cells (INPCs) . Methods INPCs were cultured in 6-well plates and were randomly divided into 5 groups ( n = 6 each) : group I was not transfected with any plasmid (group INPC); group Ⅱ was transfected with control plasmid (group INPC/CMV); group Ⅲ was transfected with plasmid RcCMV-p50 (group INPC/p50); group Ⅳ was transfected with plasmid RcCMV-p65 (group INPC/p65) and group V was transfected with plasmid RcCMV-p50 and RcCMV-p65 (group INPC/p50p65). Group INPC/CMV ( H ), INPC/p50 (Ⅲ) and INPC/p65 (Ⅳ) were screened by G418, and the positive clones were then cultured for 3-4 weeks. The transcription of p50 mRNA or p6S mRNA was detected by RT-PCR. The NF-κB activity was measured by luciferase reporter gene assay. The cell apoptosis was measured by annexin V/PI staining. In group INPC/p50p65 and group INPC/p65, the cultured positive clone was transiently transfected with plasmid RcCMV-p50. Two days after transfection, the same measurement was performed in group INPC/pS0p65 and the other groups. Results The expression of p50 mRNA was significantly increased in group INPC/p50 and INPC/p50p65 as compared with the other groups ( P < 0.05) . The expression of p65 mRNA, the NF-κB activity and the apoptotic rate were significantly increased in group INPC/p65 and INPC/p50p65 as compared with the other groups ( P < 0.05). Conclusion Enhanced NF-κB activity can increase immortalized neural progenitor cell apoptosis.