Effects of PDS on rat brain cortical nuclear factor kappa B in LPS shock

AIM:To explore the molecular mechanism of brain tissue injury induced by lipopolysaccharide (LPS),the effects of panaxadiol (PDS) on the expression of nuclear factor kappa B (NF-κB) in cerebral cortex of rat with LPS shock were studied. METHODS:Rats were randomly divided into LPS roup,LPS+dexamethasone group,LPS+PDS group and control group. The DNA binding activity and protein expression of NF-κB were observed. These indices were assayed at 1 h and 4 h after intravenous injection of LPS (4 mg·kg^-1). RESULTS:EMSA showed that PDS inhibited NF-κB DNA-binding activity in nuclear extracts at both 1 h and 4 h after LPS injection,compared with the LPS group (P<0.01). Western blotting showed that PDS down-regulated the expression of p65 and p50 protein in the nuclear extracts compared with the LPS group. However,the expression of p65 and p50 protein from cytosolic extracts did not show any significant change. CONCLUSION:PDS may alleviate brain injury by inhibiting NF-κB activation.     

Ischemia-reperfusion injury following hepatic portal occlusion increases brain excitatory amino acids and NMDAR mRNA expression in rats

AIM: To explore the changes of excitatory amino acids and N-methyl-D-aspartate receptor (NMDAR) in brain undergoing ischemia-reperfusion injury following hepatic portal occlusion (HPO) in vivo.METHODS: The electrolytes and pH of portal vein blood,the content of Glu and Asp in brain,and the expression of NMDAR mRNA were studied with blood-gas analysis,HPLC and semi-quantitative RT-PCR method in two groups(HPO or sham),respectively.Three time points(6 h,12 h and 24h after reperfusion) were included.RESULTS: HPLC measure showed that the content of cortex Glu and Asp in group HPO elevated significantly after reperfusion compared with sham group, the peaks were at 6 h and 24 h ［Glu:(349±145) μg·g^-1wt,(456±203) μg·g^-1wt vs (238±24) μg·g^-1wt,(225±59) μg·g^-1wt;Asp:(134±50) μg·g^-1wt,(166±50) μg·g^-1wt vs (99±24) μg·g^-1wt,(71±20) μg·g^-1wt］.Moreover,semi-quantitative RT-PCR analysis discovered that the expression of NMDAR mRNA increased significantly ,the subunit NR1 mRNA was higher in reperfusion 6 h and last to 12 h（1.63±0.06 vs 1.18±0.05;1.73±0.06 vs 1.17±0.03）,the peak of NR2B mRNA was in 12 h (1.75±0.04 vs 1.18±0.05) ,but they did not further increase after reperfusion for 24 h.CONCLUSION: HPO increases the content of Glu and Asp and the expression of NMDAR in brain cortex.The Glu-NMDAR pathway plays a role in the mechanism for the brain injury after HPO.The products of IR injury might be the key factor to cause EAAs acumulation in synapse space.     

Serum concentration of S100-B protein in patients during CABG with or without cardiopulmonary bypass

AIM: To investigate the mutative law of the serum S100-B protein in patients undergone coronary artery bypass grafting with or without cardiopulmonary bypass (CPB-CABG or non-CPB CABG), and to compare the degree of cerebral injury in patients during CABG between the two different surgical manipulations.METHODS: 30 patients were divided into two groups: CPB-CABG group (group A) and non-CPB CABG group (group B). Every group included 15 patients. Blood from jugular vein was phlebotomized in every patients at the following 8 time points: before operation (OP), after anaesthesia, end of grafting, end of OP, 2 h after OP, 6 h after OP, 12 h after OP and 24 h after OP. The serum concentrations of S100-B protein in the samples were measured.RESULTS: The level of serum S100-B protein increased markedly at the beginning of CABG, and the peak value of group A (2.32 μg/L±0.26 μg/L) was treble higher than that in the patients in group B (0.71 μg/L±0.14 μg/L). The levels of S100-B protein tend to normal level in both groups 24 h after OP. The level of S100-B protein had notable relation with the time of CABG in group A and the manipulative time on the heart in group B.CONCLUSION: The degree of cerebral damage can be valued by investigating the mutative law of the serum S100-B protein in patients undergone CPB-CABG and non-CPB CABG. The non-CPB CABG reduces the degree of cerebral damage and avoids the functional disorder of central nerve.     

玛曲渔场几种裂腹鱼类脑的形态结构与真食性的相互关系

本文对极边扁咽齿鱼,黄河裸裂尻鱼、花斑裸鲤和厚唇重唇鱼进行了食性分析和脑的形态结构观察,并对脑结构和食性的关系作了初步探讨。认为这四种鱼类属于底层味觉食性鱼类,其中极边扁咽齿鱼和黄河裸裂尻鱼主要靠口腔、腭部味蕾觅食泥土和藻类,迷叶发达;厚唇重唇鱼主要靠触须寻找甲壳类为主的水底昆虫,面叶和小脑发达;花斑裸鲤的脑结构特征与其杂食性相适应。     

Protective effect of BNDF on vascular endothelial cells with H2O2-induced oxidative injury

AIM: To study the protective effect of brain-derived neurotrophic factor (BDNF) on vascular endothelial cells with H₂O₂-induced oxidative injury. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro, and the oxidation injury model of HUVECs was established by treatment with H₂O₂. The oxidatively injured HUVECs were cultured with different concentrations (1, 10 and 100 μg/L) of BDNF. At the same time, the control group (no injury), PBS treatment after H₂O₂ injury group and TrkB inhibitor group (with 100 μg/L BDNF and 1: 1 000 TrkB inhibitor) were also set up. The viability of the HUVECs was detected by MTT assay. The levels of LDH, MDA, SOD and GSH were measured. The releases of NO, ET-1 and ICAM-1 were analyzed by ELISA. The changes of ROS production and cell apoptosis were evaluated by flow cytometry. The protein levels of TrkB, p-TrkB, cleaved caspase-3, Bcl-2 and Bax were determined by Western blot. RESULTS: Compared with uninjured control group, in H₂O₂ oxidative injury plus PBS treatment group, the viability of the cells was decreased significantly, the LDH and MDA levels were increased significantly and the activities of SOD and GSH were decreased significantly. The NO secretion was decreased, and the ET-1 and ICAM-1 concentrations were increased significantly. The ROS content and apoptotic rate were increased significantly. The protein levels of cleaved caspase-3 and Bax were increased but Bcl-2 protein expression was decreased significantly. Compared with PBS treatment group, in H₂O₂-injured HUVECs treated with different concentrations of BDNF, the cell viability was gradually increased, the LDH and MDA levels were decreased and the activities of SOD and GSH were increased gradually. The secretion of NO was increased but ET-1 and ICAM-1 were decreased gradually. The ROS content and apoptotic rate were decreased significantly. The TrkB and p-TrkB levels were significantly increased significantly, the protein expression of cleaved-caspase 3 and Bax was decreased gradually and the Bcl-2 protein expression increased gradually. The role of BDNF was inhibited by TrkB inhibitor. CONCLUSION: BDNF protects HUVECs from oxidative injury by binding with TrkB to activate the BDNF-TrkB signaling pathways.     

昆虫生长调节剂对东亚飞蝗脑神经分泌细胞影响的研究（Ⅰ）

应用玻璃微电极技术测定结果表明：卡死克对东亚飞蝗脑神经分泌细胞自发性电活动具有明显的抑制作用。处理组４龄若虫饲毒后第４天间脑部位的Ⅱ、Ⅲ类脑神经分泌细胞数量比正常组的减少约７５％，而且细胞放电活动强度平均降低约０．５～１．０ｍｖ．振幅，放电频率平均减少约５～１０次／ｓ。     

甲状腺素与硫尿嘧啶处理第13天鸡胚对其生长发育的影响——Ⅱ.脑中甲状腺激素含量及脑重量的变化

本文应用放射免疫方法研究了不同甲状腺机能状态下,小鸡出壳前后,脑中甲状腺激素含量和脑重量的变化.结果表明:在孵化第10天的鸡胚脑中即可检测出 T_4,T_3含量,然后逐渐上升,分别在孵化第14,17天达到峰值,此后逐渐下降.3星期内小鸡 T_4,T_3平均含量分别变化于4.3～26ng/mg,0.29～1.2ng/mg 之间.脑中 rT_3含量较低,因而检测不出.在孵化第13天的受精蛋中注入甲状腺素(200ng/枚),可使脑中 T_3/T_4比值减小;而注射硫尿嘧啶(200μg/枚)却使之增加.上述处理,对小鸡出壳前后脑的增重无显著影响.     

微创血肿清除术联合亚低温疗法治疗高血压脑出血的临床研究

目的:探讨微创颅内血肿清除术及微创术联合亚低温脑保护治疗高血压脑出血的临床疗效。方法:将163例高血压脑出血患者随机分为3组:常规治疗组54例,行内科保守治疗;微创治疗组53例,在内科治疗的同时行微创颅内血肿清除术;联合治疗组56例,行微创治疗加亚低温治疗。比较3组患者之间及治疗前后神经功能缺损评分、3组治疗效果和3组治疗后3个月随访Barthel指数。结果:联合治疗组有效率为89.28%,高于微创治疗组和常规治疗组(P<0.05);联合治疗组治疗3个月患者日常生活活动能力亦高于微创治疗组和常规治疗组(P<0.05)。结论:微创颅内血肿清除术操作简单、安全可靠、损伤小、术后恢复快;亚低温具有脑保护功能,加快神经功能恢复。微创术和亚低温联合治疗高血压脑出血可明显降低病死率和致残率。     

Erythropoietin attenuates cerebral ischemia-induced cognitive dysfunction through stimulation of hippocampal CREB phosphorylation in C57BL/6 mice

AIM: To investigate the neuroprotective effect of erythropoietin (EPO) on cognitive dysfunction and neuronal injury in hippocampal CA1 region induced by cerebral ischemia in mice. METHODS: Male C57BL/6 green fluorescent protein-transgenic mice were randomly divided into 3 groups: sham operation group (sham), ischemia/reperfusion group (I/R) and EPO-treated group. Transient cerebral global ischemia was induced by bilateral common carotid artery occlusion (2-VO). The step-down test was used to measure the capacity of learning and memory of the animals in each group. Nissl staining was applied to examine the neuronal number in hippocampal CA1 region. The expression of phosphorylated cAMP response element-binding protein (pCREB) was determined by Western blotting. Alterations of dendritic morphology in hippocampal CA1 region were evaluated using laser scanning confocal microscopy and Neurolucida software. RESULTS: Transient cerebral ischemia caused deficits of spatial learning and memory, and delayed neuronal death and loss of dendritic spines in hippocampal CA1 region were also obvious. The EPO treatment significantly improved the cognitive function in cerebral ischemic mice, and the protein expression of pCREB was obviously increased. At the same time, neuronal death and loss of dendritic spines were reduced in hippocampal CA1 region. CONCLUSION: Erythropoietin increases the protein expression of pCREB, and reduces neuronal death and loss of dendritic spines. These processes may be responsible for erythropoietin-mediated neuroprotective effects and the improvement of cognitive function in cerebral ischemic mice.     

Effect of autophagy in traumatic brain injury

Autophagy is a metabolic process of eukaryotic cells. When lacking of nutrient and energy, the cells obtain biosynthetic materials by degrading the organelles and recycling the proteins to maintain homeostasis. Traumatic brain injury (TBI) is a common kind of mechanic injury, usually with a poor outcome. Accumulated evidence indicates that the activity of autophagy increases after TBI. However, its implication for nervous tissue is still controversy. On one hand, autophagy exerts a protective effect on the neural cells. On the other hand, autophagy can also induce cell death exacerbating neural injury. This review focuses on the processes of autophagy and its roles in TBI, which may provide some novel therapeutic strategies.