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find Keyword "髓鞘碱性蛋白" 3 results
  • EFFECT OF CHONDROITINASE ABC ON AXONAL MYELINATION AND GLIAL SCAR AFTER SPINAL CORD INJURY IN RATS

    Objective To investigate the effects of chondroitinase ABC (ChABC) on axonal myelination and glial scar after spinal cord injury (SCI) in rats. Methods Seventy-two adult male Sprague Dawley rats were randomly assigned into ChABC treatment group (group A), saline treatment group (group B), and sham operation group (group C), 24 rats in each group. In groups A and B, the SCI model was established with modified Allen’s method and then the rats of groups A and B were administrated by subarachnoid injection of 6 μL ChABC (1 U/mL) and saline respectively at 1 hour after injury and every day for 1 week; the rats of group C served as control, which canal was opened without damage to spinal cord. At 1, 7, 14, and 28 days after operation, the locomotor functions were evaluated according to the Basso-Beattie-Bresnahan (BBB) score scale; and the spinal cord samples were harvested for HE staining, Nissl staining, and immunohistochemistry analysis to detect the change of myelin basic protein (MBP), growth associated protein 43 (GAP-43), and glial fibrillary acidic protein (GFAP) of the injured spinal cord. Results At different time points, the BBB score of group C was significantly higher than those of groups A and B (P lt; 0.05), and the BBB score of group A was significantly better than that of group B at 14 and 28 days after operation (P lt; 0.05). HE staining and Nissl staining showed that the morphous and the neuron number of the remainant injured spinal cord in group A were better than those in group B. The integral absorbance (IA) values of MBP and GAP-43 and the positive area of GFAP after SCI in groups A and B were significantly higher than those in group C at different time points (P lt; 0.05), and the IA values of MBP and GAP-43 were significantly higher in group A than those in group B at 7, 14, and 28 days after operation (P lt; 0.05), but the positive area of GFAP was significantly smaller in group A than that in group B (P lt; 0.05). Conclusion The ChABC can effectively improve the microenvironment of the injured spinal cord of rats, enhance the expressions of MBP and GAP-43, and inhibit the expression of GFAP, which promotes the axonal regeneration and myelination, attenuate glial scar formation, and promote the recovery of nerve function.

    Release date:2016-08-31 04:06 Export PDF Favorites Scan
  • Changes of Neuron-specific Enolase and Myelin Basic Protein in the Serum and Cerebrospinal Fluid in Patients with Epilepsy after Single Episodes

    【摘要】 目的 探讨单次癫痫发作是否会引起脑损伤。 方法 2007年6月-2009年11月,采用电化学发光法检测癫痫发作后24 h内40例和对照组40例患者血清和脑脊液中神经元特异性烯醇化酶(neuron-specific enolase,NSE)水平,采用ELISA法测定其血清和脑脊液中髓鞘碱性蛋白(myebin bosic protein,MBP)水平。 结果 癫痫组血清和脑脊液中NSE水平明显高于对照组(Plt;0.01);癫痫组血清MBP水平与对照组比较差异无统计学意义(Pgt;0.05);癫痫组脑脊液中MBP水平高于对照组(Plt;0.05)。 结论 单次癫痫患者血清和脑脊液中NSE明显升高,脑脊液中MBP升高,提示单次癫痫发作可导致神经元损伤。【Abstract】 Objective To detect the possibility of brain damage in the epileptic patients after single episodes. Methods The levels of neuron-specific enolase (NSE) in serum and cerebrospinal fluid (CSF) in 40 patients with single episodes within 24 hours after seizures from June 2007 to November 2009 were determined respectively by electrochemiluminescence. Another 40 healthy individuals were enrolled as the control. The levels of myelin basic protein (MBP) were determined by enzyme-linked immunosorbent assay. Results The levels of NSE in the serum and CSF in epileptic group within 24 hours after seizures were significantly higher than those in the control group (Plt;0.01), and the levels of MBP in the serum in the two group didn′t differ much (Pgt;0.05). The levels of MBP in CSF in epileptic group were significantly higher than those in the control group (Plt;0.05). Conclusion After single episodes, the levels of NSE in serum and CSF and the levels of NSE in CSF increase,which suggests that single episodes may lead to neuronal damage.

    Release date:2016-09-08 09:52 Export PDF Favorites Scan
  • Changes in Level of Myelin Basic Protein,TNF-α and IL-6, and Their Correlative Study in Experimental Rat of Pancreatic Encephalopathy

    ObjectiveTo discuss the changes of myelin basic protein (MBP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in serum and cerebrospinal fluid of experimental pancreatic encephalopathy rat model, analyze the relationship between each factor and the occurrence and development of pancreatic encephalopathy, and to provide the experimental basis for clinical diagnosis and treatment of pancreatic encephalopathy. MethodsSelecting 40 SD rats were randomly divided into sham operation group (SO group, n=10) and pancreatic encephalopathy group (PE group, n=30), respectively by the duodenal papilla retrograde pancreatic puncture injection of saline solution or 5% sodium taurocholic acid induced rat pancreatic encephalopathy model were set up. The rats in SO group were sacrificed on 1 d, and the PE group were sacrificed ten rats on 1 d, 3 d, and 7 d, respectively after surgery. The brain and pancreatic tissues of rats in each group were taken to observe the pathological changes of the rats and the brain white blood cells within microvessels gathered and coanda phenomenon. The water content of brain tissues, and the contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid were detected. ResultsThe changes of brain nerve cell edema and nerve fiber demyelination were obvious in PE group rats after surgery with the extension of time. The contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid on 1 d, 3 d, and 7 d after surgery in PE group were significantly higher than that SO group (P<0.05), and gradually increased with the extension of time. But by two two compared, the change trend of the above three indicators were different. ConclusionsMBP, TNF, and IL-6 on the occurrence and development of brain damage of pancreatic encephalopathy play a synergistic effect. To detecte the MBP, TNF-a, and IL-6 content in blood and cerebrospinal fluid could be diagnosed and evaluated the pancreatic encephalopathy.

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