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The Effects Of Selenium Deficiency Diet On CREB And Nuclear Matrix Proteins In Brain Of Developing Rat

Posted on:2005-03-15Degree:MasterType:Thesis
Country:ChinaCandidate:Y Q GengFull Text:PDF
GTID:2144360125962587Subject:Forensic medicine
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Object To observe the changes of lipid peroxide in the cortex and hippocampus of developing rat induced by selenium deficiency diet and study the neuron function by the content and activity detection of cAMP Response Element-Binding Protein (CREB) in cortex and hippocampus. To study the alteration of NMPs components. Material and method Groups of healthy adult SD rats with equal male and female at random were fed with selenium deficiency and selenium adequate food. The third generation at 21 days of age were killed and the cortex and hippocampus were dissected on ice rapidly. The contents of MDA were assayed by 2-thiobarbituric acid (TBA) test. The expression of CREB and p-CREB were examined by western blot in the extracted total protein from cortex and hippocampus. The expression and the location of CREB and p-CREB were further explored in different kind of neuron in the same region of brain by paraffin brain section immunohistochemistry. The expression of p-CREB was also detected from the extracted NMPs of rat brain by western blot. The component of the NMPs between two groups were analysed and compared by High Performance Capillary Electrophorisis(HPCE). Result The content of MDA in the cortex and hippocampus of selenium deficiency group was much higher than that of the control group(control cortex MDA=0.31 + 0.13, selenium deficiency cortex MDA=0.66 + 0. 10, P<0. 05;control hippocampus MDA=0. 42 + 0. 11 , selenium deficiency hippocampus MDA=0.89 + 0.066);Thedetection of CREB and p-CREB from the total protein showed that the expressions of selenium deficiency group were lower than that of control group. The grey degree of CREB positive cells in selenium deficiency cortex and hippocampus that were examined by immunohistochemistry increased (control cortex=119.62 ?8.35, selenium deficiency cortex = 144.67+ 16.67, P<0. 05 and control hippocampus = 123.13?.74, selenium deficiency hippocampus=150.16?3.80, P<0.05). The p-CREB positive cells decreased in cortex and the area CA1 in hippocampus of selenium deficiency (control cortex= 171.89 + 63.062, selenium deficiency cortex = 109.44 + 38. 41,P<0.01 and control hippocampus = 28.14 + 9.25, selenium defiency hippocampus=8.67+ 1.53 P<0.05. ) The decline of the expression of p-CREB in granular cells control =157.17 + 44.80, selenium deficiency = 29.40+ 13.11 ,P<0.01) was much greater than in glial cells (control=68.80+13.78, selenium defiency=51.50 + 14 86, P>0.05) . The NMPs can be separated by CE with three or four peaks. There was one peak, which occurred at about 9 min separation, showed significant drop in the selenium deficiency groupConclusion (1) The decline of oxidant metabolism in the developing cortex and hippocampus can be induced by selenium deficiency diet. (2) The reduction of the expression of CREB and p-CREB reflected the decreased cortex and hippocampus neuron functions. It is indicated that selenium deficiency maybe one of the reasons to decline the learning and memory ability. (3) The alteration of NMPs can be induced by selenium deficiency.
Keywords/Search Tags:Selenium, Brain, CREB, High performance capillary electrophoresis, Nuclear matrix proteins
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