| Background and Objective: Selenium was an essential trace element for growth and development of human body. It had very important function. The Se-deficient caused the selenoenzyme activity decrease and the function of eliminating oxidant radical, protect the biological membrane, detoxification and immunity lessen. It was possible to affect the brain development. After iodine supplemented at diet for more than 20 years, and the situation of I-deficiency was basically wiped off. But there are still lots of subcretinism children are born every year. The purpose of study is to know the Se-deficiency was whether or another significant factors for the intellect, and the scholar payed more and more attention to the relationship between Se and neural differentiation and growth. There had some report about Se affected the neural cell development in vitro. But how Se affects the brain morphological development in vivo, and how the Se&I combined deficiency? There is a litter report. In these study we utilized the P4 , P21 brain samples from Se-deficient and I-deficient F3 rats to research the morphological changes, neural mature differentiated protem-GFAP, NSE CNPase andneurotrophic factors BDNF expression at hippocampus(Hp). Material and Method: The experimented animals were from Se-deficient, I-deficient F3 rat. The animals were divided four groups: Se-deficient; I-deficient; Se & I-deficient and controlled (supplement Se & I) groups. We respectively took P4(4 per group) and P21(6 per group) brain samples fixed embedded-sliced made HE Nissl PAS stain, GFAP NSE CNPase BDNF immunohistochemistry. In addition, we extracted total protein from the P21 fresh hippocampus tissue(4 per group) to detect the GFAP NSE CNPase BDNF protein expression by Western Blot technique. Results:1 Morphological changed: Contrasted to the controlled group, cortex cellular migrative speed and dentate gyrus (DG) growth were slower at the Se-, I- and Se-I- , delamination of cortex was unclear; at P21, Se-, I-and Se-I- groups had higher cell density at cortex and polarity of arrangement was worse than the controlled group. The changes were worse at I- and Se-I- than Se-.2 Stereology of Hp: at CA1 regions, the numerical value of Vv SF N/P at controlled group was lower than I-(P<0.05) and Se-I-(P<0.01), and Sv was higher; Se- had bigger figure than controlled group(P<0.01) at SF and N/P, and Se- had higher Sv than I-, SeI-(P0.01\). At CA3 regions, the difference of four indexes between controlled group with others hadstatistic signification; Se- had higher Sv than I-(P<0.05), Se- had lower SF(P<0.01) N/P(0.05) and higher Sv(P<0.01) than Se--. At DG regions, the value of SF N/P at controlled group were lowest than other groups(P<0.01); there was no difference among Se I- and Se-I-. The layer and thickness increased at Se- and I- than controlled group, but the changes at Se-I- was not obvious. The results indicated Se- I- and Se-I-causes Hp cellular dysplasia.3 Neural mature differentiated protein expression: The positive cell of GFAP and gray intensity of control group were higher than others at CA1 and DG regions (P<0.01), at CA3 regions are higher than Se-, Se-I-(P<0.01). Western Blot reveals the GFAP protein concentration is highest at control group, the difference among othere groups were no significant. The gray intensity of NSE at control group is higher than I-and SeI-(P<0.01), there are no difference with Se-. Western Blot showed there were differences among the groups, consistents with immunohistochemistry results. CNPase positve cell express at Hp and cotex. The results of accounting positive cell at CA3 were different. It shows I- and Sel- had more positive cell than control and Se- group. And the gray of positive fibers were more intensive at cortex of I- and Sel-group, the projecting areas were wider.4 Neurotrophic factor express: The immunohistochemistry showed BDNF commonly expressed at Hp cortex and midbrain. The controlledgroup had more gray intensity than Se- and Sel- group at hippocampal p... |
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