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.
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.