We have found that Batroxobin plays a protactive role in ischemic brain injury, which attracted us to investigate the effect of Batroxobin on apoptosis of neurons during cerebral ischemia and reperfusion. The apoptotic cells in ischemic rat brains at different reperfusion intervals were tested with method of TdT-mediated dUTP-DIG nick end labeling (TUNEL) and the effect of Batroxobin on the apoptosis of neurons was studied in left middle cerebral artery (LMCA) occlusion and reperfusion in rat models (n=18). The results showed that few scattered apoptosis cells were observed in right cerebral hemispheres after LMCA occlusion and reperfusion, and that a lot of apoptosis cells were found in left ischemic cortex and caudoputamen at 12h reperfusion, and they reached peak at 24h~48h reperfusion. However, in the rats pretreated with Batroxobin, the number of apoptosis cells in left cerebral cortex and caudoputamen reduced significantly and the neuronal damage was much milder at 24h reperfusion than that of saline-treated rats. The results indicate that administration of Batroxobin may reduce the apoptosis of neurons induced by cerebral ischemia and reperfusion and afford significant cerebroprotection in the model of focal cerebral ischemia and reperfusion.

The traditional Chinese medicine Buyang Huanwu Decoction has been shown to improve the neu-rological function of patients with stroke. However, the precise mechanisms underlying its effect remain poorly understood. In this study, we established a rat model of cerebral ischemia by middle cerebral artery occlusion and intragastrical y administered 5 g/kg Buyang Huanwu Decoction, once per day, for 1, 7, 14 and 28 days after cerebral ischemia. Immunohistochemical staining revealed a number of cel s positive for the neural stem cel marker nestin in the cerebral cortex, the subven-tricular zone and the ipsilateral hippocampal dentate gyrus in rat models of cerebral ischemia. Buyang Huanwu Decoction significantly increased the number of cel s positive for 5-bromodeoxyuridine (BrdU), a cel proliferation-related marker, microtubule-associated protein-2, a marker of neuronal differentiation, and growth-associated protein 43, a marker of synaptic plasticity in the ischemic rat cerebral regions. The number of positive cel s peaked at 14 and 28 days after intragastric administration of Buyang Huanwu Decoction. These findings suggest that Buyang Huanwu Decoction can promote the proliferation and differentiation of neural stem cel s and hance synaptic plasticity in ischemic rat brain tissue.

Paired immunoglobulin-like receptor B (PirB) is a functional receptor of myelin-associated in-hibitors for axonal regeneration and synaptic plasticity in the central nervous system, and thus suppresses nerve regeneration. The regulatory effect of PirB on injured nerves has received a lot of attention. To better understand nerve regeneration inability after spinal cord injury, this study aimed to investigate the distribution of PirB (via immunolfuorescence) in the central nervous system and peripheral nervous system 10 days after injury. Immunoreactivity for PirB increased in the dorsal root ganglia, sciatic nerves, and spinal cord segments. In the dorsal root ganglia and sciatic nerves, PirB was mainly distributed along neuronal and axonal membranes. PirB was found to exhibit a diffuse, intricate distribution in the dorsal and ventral regions. Immunore-activity for PirB was enhanced in some cortical neurons located in the bilateral precentral gyri. Overall, the ifndings suggest a pattern of PirB immunoreactivity in the nervous system after uni-lateral spinal transection injury, and also indicate that PirB may suppress repair after injury.

Many studies have examined motor impairments using voxel-based lesion symptom mapping, but few are reported regarding the corresponding relationship between cerebral cortex injury and lower limb motor impairment analyzed using this technique. This study correlated neuro-nal injury in the cerebral cortex of 16 patients with chronic stroke based on a voxel-based lesion symptom mapping analysis. Neuronal injury in the corona radiata, caudate nucleus and putamen of patients with chronic stroke could predict walking speed. The behavioral measure scores were consistent with motor deifcits expected after damage to the cortical motor system due to stroke. These ifndings suggest that voxel-based lesion symptom mapping may provide a more accurate prognosis of motor recovery from chronic stroke according to neuronal injury in cerebral motor cortex.

Supratentorial cerebral infarction can cause functional inhibition of remote regions such as the ce-rebel um, which may be relevant to diaschisis. This phenomenon is often analyzed using positron emission tomography and single photon emission CT. However, these methods are expensive and radioactive. Thus, the present study quantified the changes of infarction core and remote regions after unilateral middle cerebral artery occlusion using apparent diffusion coefficient values. Diffu-sion-weighted imaging showed that the area of infarction core gradual y increased to involve the cerebral cortex with increasing infarction time. Diffusion weighted imaging signals were initial y in-creased and then stabilized by 24 hours. With increasing infarction time, the apparent diffusion coefficient value in the infarction core and remote bilateral cerebel um both gradual y decreased, and then slightly increased 3-24 hours after infarction. Apparent diffusion coefficient values at mote regions (cerebel um) varied along with the change of supratentorial infarction core, suggesting that the phenomenon of diaschisis existed at the remote regions. Thus, apparent diffusion coeffi-cient values and diffusion weighted imaging can be used to detect early diaschisis.

被动运动加氦-氖激光治疗急性脑梗死偏瘫50例

BACKGROUND: Passive exercise can promote plastic de-velopment of cerebral cortex function with afferent stimuli received by receptors and recover lost functions. Utility of Helium-neon laser can protect neurons.

人巨细胞病毒先天性感染胎鼠大脑皮质钙调素基因mRNA表达的研究

目的研究先天性人巨细胞病毒(HCMV)感染致脑损害后钙调素(calmodulin,CaM)基因mRNA表达的改变,以探讨先天性HCMV感染所致脑损害的机制.方法选用10周龄Balb/c小鼠,雌雄小鼠腹腔内分别注射1.0ml、0.5ml、0.25ml HCMV后合笼交配以建立先天性HCMV中枢神经系统(CNS)感染小鼠模型,对照鼠腹腔注射1.0ml RPMI 1640液.剖腹取21天胎龄小鼠大脑皮质,以自行设计的CaM cDNA编码区的一对引物与一条CaM特异性探针,分别用逆转录聚合酶链反应(RT-PCR)技术检测CaM mRNA相对含量、用原位杂交检测大脑皮质细胞内相应mRNA的表达及定位.结果母鼠腹腔内接种HCMV量为1.0ml与0.5ml的临产胎鼠大脑皮质分离出相应病毒,病理学检查等确认发现了侵袭性脑膜脑炎性病理改变,证实HCMV可经小鼠宫内传播至胎鼠CNS.1.0ml组与0.5ml组胎鼠RT-PCR产物浓度明显高于0.25ml组及对照组,而1.0ml组与0.5ml组间亦有明显差异.电泳结果显示对照组与0.25ml组胎鼠未见阳性条带,而1.0ml组胎鼠特异性条带信号强于0.5ml胎鼠,仅略低于同组母鼠.原位杂交显示CaM mRNA不但出现在1.0ml组胎鼠大脑皮质大神经元胞核及胞浆内,在中小神经元及胶质细胞的胞核及胞浆亦有高密度表达,阳性细胞的突起中亦有弱信号存在.结论提示先天性感染HCMV胎鼠大脑皮质内CaM mRNA表达量明显增加,且神经元及胶质细胞均有表达,并与感染剂量有依赖关系.提示CaM mRNA表达增高可能直接参与了HCMV先天性感染脑损害的过程.

共聚焦激光扫描显微镜(MRC600)活体观测川芎嗪和去甲基肾上腺素对休克状态下家兔大脑皮质内微循环的影响

脑微循环障碍对休克起主导作用,是其发病重要环节的典型例证之一[1].川芎嗪是目前临床上常用的活血化瘀、抗休克、改善微循环的治疗手段之一.

氯胺酮,咪唑安定,硫喷妥钠和异丙酚对大鼠皮层脑片缺血性损伤的作用

AIM: To compare the effects of ketamine, midazolam, thiopental, and propofol on brain ischemia by the model of oxygen-glucose deprivation (OGD) in rat cerebral cortical slices. METHODS: Cerebral cortical slices were incubated in 2 % 2,3,5-triphenyltetrazolium chloride (TTC) solution after OGD, the damages and effects of ketamine,midazolam, thiopental, and propofol were quantitativlye evaluated by ELISA reader of absorbance (A) at 490 nm,which indicated the red formazan extracted from slices, lactic dehydrogenase (LDH) releases in the incubated supernate were also measured. RESULTS: Progressive prolongation of OGD resulted in decreases of TTC staining.The percentage of tissue injury had a positive correlation with LDH releases, r=0.9609, P＜0.01. Two hours of reincubation aggravated the decrease of TTC staining compared with those slices stained immediately after OGD (P＜0.01). These four anesthetics had no effects on the TTC staining of slices. Ketamine completely inhibited the decrease of A value induced by 10 min of OGD injury. High concentrations of midazolam (10 μmol/L) and thiopental (400 μmol/L)partly attenuated this decrease. Propofol at high concentration (100 μmol/L) enhanced the decrease of A value induced by 10 min of OGD injury (P＜0.01). CONCLUSION: Ketamine, high concentration of midazolam and thiopental have neuroprotective effects against OGD injury in rat cerebral cortical slices, while high concentration of propofol augments OGD injury in rat cerebral cortical slices.