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Objective To explore the protective effect and molecular mechanism of dl-3-n-butylphthalide (NBP) against oxygen-glucose deprivation induced by sodium hydrosulfite in PC12 cells at proteomic level.Methods PC12 cells impaired by serum-free culture media with sodium hydrosulfite were used as the cell models ofhypoxia,and the protective effects of NBP on hypoxic cells were observed.Methyl thiazolyl tetrazolium (MTT) assay was used to measure the viabilities of PC12 cells.Proteomic technique was employed to identify the differential expression proteins.Results Following the increment of NBP concentrations,the cell absorbance (A) value increased gradually (the PC12 cell apoptosis reduced gradually); when the NBP concentration reached 5 mol/L,their cell A value was significantly different as compared with that of cells without adding NBP (P＜0.05).By using proteomics methods,17 differentially-expressed protein spots in the cells without adding NBP and cells with NBP were identified; most of proteins were cytoskeleton proteins,apoptosis related proteins and oxidative stress related proteins.Conclusion NBP can reduce neuronal apoptosis induced by hypoxia,and cytoskeletal proteins,apoptosis-related proteins and oxidative stress related proteins may role in protection of NBP on ischemic neurons.
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Objective To investigate the molecular mechanism of corticobasal degeneration and search the protein markers ofdiagnoseis and treatment of this disease. Methods The brains of subjects died without clinical or pathological involvement of nervous system (n=4) and brains of patients with corticobasal degeneration (n=4) were obtained at autopsy. Tissues samples were cut from the frontal and temporal lobes, and the striatum. Histological changes of the tissue samples were observed by HE staining, Gallyas-Braak silver staining and Tau protein immunohistochemistry. The samples extracted from the frontal lobe were performed dimensional electrophoresis with immobilized pH gradient (IPG)isoelectric focusing electrophoresis as the first dimension and with vertical sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) as the second dimension; the maps were visualized by Coomassie brilliant blue staining and analyzed with ImageMaster 2D Elite software; the protein profiles were in-gel digested and identified by mass spectrometry (MALDI-TOFTOF). Results Significant neuron loss in the temporal lobe of patients with corticobasal degeneration was noted by HE staining, with mass proliferation of gliocyte in the temporal lobe; sphere-like entanglement in the striatum was noted by Gallyas-Braak silver staining and Tau immunohistochemistry. Fourteen protein spots in the brains of patients with corticobasal degeneration were differentially expressed as compared with those in age-matched nondemented control brains; the expression of 9 proteins (cofilin, uracil DNA glycosylase,Cu-Zn superoxide dismutase, isocitrate dehydrogenase subunit, synaptotagmin Ⅰ, thioredoxin peroxidase 1, glial fibrillary acidic protein, P25 alpha and peroxiredoxin 5) in brains of patients with corticobasal degeneration was up-regulated as compared with that in the normal brain tissue (P＜0.05); the expression of 5 proteins (carbonyl reductase [NADPH] 1, ferritin heavy chain, peptidyl-prolyl cis-trans isomerase A,serum albumin precursor and dihydropyrimidinase-related protein 2) in brains of patients with corticobasal degeneration was down-regulated as compared with that in the normal brain tissues (P＜0.05).Conclusion We get a number of related-proteins of corticobasal degeneration. Some proteins are quite useful in discovering the molecular mechanisms of corticobasal degeneration and may be helpful in the ealry diagnosis and treatment of corticobasal degeneration and in the development of new medicine.
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<p><b>OBJECTIVE</b>To evaluate the clinical results of continuing skeletal traction and impaction granular bone grafting via window in femoral neck for the treatment of avascular necrosis of femoral head.</p><p><b>METHODS</b>From August 2000 to October 2004, 23 patients (35 hips) with femoral head necrosis were treated by continuing skeletal traction and impacting granular bone grafting via bone window on femoral neck. There were 18 males, 5 females, with an average age of 32 years ranging from 19 to 52 years, which included 7 hips of stage II, 28 hips of stage III. All patients had various degrees of hip joint pain and suffered from limited hip motion. The necrotic bone, granulation tissue and hardening zone were completely cleaned via bone window on the femoral neck. The autogenous granular iliac bone was grafted, and impacted persistently. Skeletal traction through femur condyles was applied continually after the operations. The effects before and after operation were compared by the hip pain, function, joint activity and X-ray.</p><p><b>RESULTS</b>Regular follow-up was carried out after the patients were dismissed from the hospital. The follow-up period was 6 months, 1 year, 2 years, 3 years, 4 years, 5 years respectively. According to Wang's standard, the average score was increased from (52.66 +/- 12.53) preoperatively to (88.94 +/- 5.84) preoperatively at half a year, (89.78 +/- 6.18) at 1 year, (86.37 +/- 7.46) at 2 years, (84.08 +/- 7.57) at 3 years, (83.76 +/- 8.08) at 4 years, and (76.83 +/- 8.98) at 5 years. Scores of operation were greatly increased and the difference had statistical significance.</p><p><b>CONCLUSION</b>Continuing skeletal traction after the operation, completely cleaning the necrotic bone and impacting granular bone grafting via window on femoral neck can greatly raise the satisfactory rate of clinical effect and delay the progression of disease for avascular necrosis of femoral head.</p>