Objective To investigate the impact of propofol on neuronal damage in neonatal rats with ischemic hypoxic brain injury（HIBD） by regulating sirtuin 1（SIRT1）/high mobility group protein 1（HMGB1）/nuclear transcription factor-κB（NF-κB） signaling pathway in ischemic hypoxic brain injury（HIBD）. Methods SD neonatal rats were taken to construct hypoxic-ischemic brain injury（HIBD） model by Rice-Vannucci method, and they were randomly grouped into model group, low-dose propofol group（5 mg/kg）, and high-dose propofol group（10 mg/kg）, EX527 group（5 mg/kg）, and high-dose propofol（10 mg/kg）+EX527（5 mg/kg） group, 15 in each group, another 15 newborn rats were regarded as the sham operation group. After group and intervention with propofol and EX527, the cognitive function of rats was detected by platform jump test. Brain water content of rats was measured. Nissl staining was applied to detect the number of neurons in the hippocampus of rats in each group. Transmission electron microscopy was applied to observe the ultrastructure of rat hippocampal neurons.The kit was applied to detect the levels of inflammatory mediators tumor necrosis factor-α（TNF-α）, inducible nitric oxide synthase（iNOS）, and oxidative stress factors total antioxidant capacity（TAC） and malondialdehyde（MDA） in serum and brain tissue of rats in each group. Western blotting was applied to detect the relative expression of SIRT1/HMGB1/NF-κB pathway in brain tissue of rats in each group. Results Compared with the sham-operation group, the ultrastructure of hippocampal neurons in the model group was severely damaged, the platform latency, the number of hippocampal neurons, the levels of TAC in serum and brain tissue, and the expression of SIRT1 protein in brain tissue were obviously decreased（P＜0.05）. The brain water content, the number of platform mistakes, the levels of TNF-α, iNOS, and MDA in serum and brain tissue, the expression of HMGB1 protein in brain tissue, and p-NF-κB p65/NF-κB p65 were obviously increased（P＜0.05）. Compared with the model group, the ultrastructural damage of hippocampal neurons in the low-dose propofol group and the high-dose propofol group were alleviated, the platform latency, the number of hippocampal neurons, the levels of TAC in serum and brain tissue, and the expression of SIRT1 protein in brain tissue were obviously increased（P＜0.05）. The brain water content,the number of platform mistakes, the levels of TNF-α, iNOS, and MDA in serum and brain tissue, the expression of HMGB1protein in brain tissue, and p-NF-κB p65/NF-κB p65 were obviously decreased（P＜0.05）. The ultrastructural injury of hippocampal neurons in the high-dose propofol group were further alleviated compared with those in the low-dose propofol group,the platform latency, the number of hippocampal neurons, the levels of TAC in serum and brain tissue, and the expression of SIRT1 protein in brain tissue were obviously further increased（P＜0.05）. The brain water content, the number of platform mistakes, the levels of TNF-α, iNOS, and MDA in serum and brain tissue, the expression of HMGB1 protein in brain tissue,and p-NF-κB p65/NF-κB p65 were obviously further decreased（P＜0.05）. The ultrastructural injury of hippocampal neurons in the EX527 group were aggravated, the platform latency, the number of hippocampal neurons, the levels of TAC in serum and brain tissue, and the expression of SIRT1 protein in brain tissue were obviously decreased（P＜0.05）. The brain water content,the number of platform mistakes, the levels of TNF-α, iNOS, and MDA in serum and brain tissue, the expression of HMGB1protein in brain tissue, and p-NF-κB p65/NF-κB p65 were obviously increased（P＜0.05）. Compared with the high-dose propofol group, the ultrastructural damage of the hippocampal neurons in the high-dose propofol+EX527 group were aggravated,the platform latency, the number of hippocampal neurons, the levels of TAC in serum and brain tissue, and the expression of SIRT1 protein in brain tissue were obviously decreased（P＜0.05）. The brain water content, the number of platform mistakes,the levels of TNF-α, iNOS, and MDA in serum and brain tissue, the expression of HMGB1 protein in brain tissue, and p-NF-κB p65/NF-κB p65 were obviously increased（P＜0.05）. Conclusion Propofol can inhibit the activation of HMGB1/NF-κB signaling by up-regulating SIRT1, thereby inhibiting inflammation and oxidative stress, and reducing neuronal damage in neonatal rats with HIBD.

目的 探讨山莨菪碱联合丹参在美尼尔综合征(MS)治疗中的效果.方法 将临床确诊的60例MS患者随机分为观察组30例和对照组30例,对照组给予营养脑细胞,对症治疗,观察组在对照组的基础上将山莨菪碱注射液10～20mg、复方丹参注射液20～40ml加入10%葡萄糖液250ml静滴,1次/d,7d为一个疗程,比较两组的总治愈率.结果 观察组治疗的总有效率为93.3%,对照组的总有效率为50.0%,两组比较有显著性差异(P<0.01).结论 山莨菪碱联合丹参治疗美尼尔综合征效果好.