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低硒對(duì)F344大鼠子代神經(jīng)行為發(fā)育和海馬神經(jīng)前體細(xì)胞分化、成熟蛋白表達(dá)的影響

發(fā)布時(shí)間:2018-09-10 05:54
【摘要】:背景與目的 硒是人和動(dòng)物生命活動(dòng)所必需的微量元素。硒缺乏會(huì)引起含硒酶活性降低,氧自由基清除受阻、內(nèi)分泌紊亂等一系列機(jī)體功能障礙,其對(duì)神經(jīng)系統(tǒng)的影響也越來越引起學(xué)者們的重視。 前期本課題組建立了人工膳食低硒、低碘和聯(lián)合低硒低碘喂養(yǎng)的SD大鼠動(dòng)物模型,并歷時(shí)近三年繁衍至仔四代,研究結(jié)果發(fā)現(xiàn),仔三代、四代低硒大鼠已經(jīng)表現(xiàn)出不同程度體格和神經(jīng)發(fā)育延遲、腦內(nèi)EGFR/MAPK信號(hào)傳導(dǎo)通路有一定影響、但Morris水迷宮空間記憶能力沒有明顯影響等。 本實(shí)驗(yàn)在前期研究的基礎(chǔ)上,再次通過人工低硒飼料喂養(yǎng)F344近交系大鼠復(fù)制低硒動(dòng)物模型,深入細(xì)致研究其子代出生后早期不同時(shí)間點(diǎn)4d,7d,14d,21d的含硒酶GPx(glutathione peroxidase,谷胱甘肽過氧化物酶)活性變化、早期神經(jīng)行為發(fā)育、子代發(fā)育期大鼠開場行為和Morris水迷宮空間記憶能力表現(xiàn)。并通過檢測腦神經(jīng)細(xì)胞形態(tài)發(fā)育、海馬神經(jīng)前體細(xì)胞標(biāo)記蛋白(nestin)、增殖細(xì)胞核抗原(PCNA)、膠質(zhì)細(xì)胞分化成熟蛋白——膠質(zhì)纖維酸性蛋白(glial fibrillary acidic protein,,GFAP)和2’,3’-環(huán)核甘酸3’-磷酸二酯酶(2,3-cyclic nucleotide,3-phosphodiesterase,CNPase)的表達(dá)情況,從發(fā)育,行為,功能到海馬局部形態(tài)結(jié)構(gòu)和分化、成熟蛋白的表達(dá),進(jìn)一步深入探討低硒對(duì)早期神經(jīng)發(fā)育的影響,尋找這一影響的形態(tài)結(jié)構(gòu)和功能基礎(chǔ)。 方法 1 復(fù)制F344低硒大鼠動(dòng)物模型 參照本課題組已成功建立的人工膳食SD低硒大鼠模型
[Abstract]:Background and objective selenium is an essential trace element for human and animal life. Selenium deficiency can lead to the decrease of the activity of selenase, the elimination of oxygen free radicals, endocrine disorders and a series of functional disorders. The effect of selenium deficiency on nervous system has been paid more and more attention by scholars. In the early stage of the study, the SD rat model of artificial diet with low selenium and iodine and low selenium and iodine was established, which lasted for nearly three years to reproduce to the fourth generation of the offspring. The results showed that the third generation, the third generation. Four generations of low selenium rats have shown different degrees of physical and neurodevelopmental delay, brain EGFR/MAPK signal transduction pathway has a certain effect, but Morris water maze spatial memory ability has no significant effect. On the basis of previous studies, the animal model of selenium deficiency was established by feeding F344 inbred strain rats with artificial low selenium diet. The activity of selenase GPx (glutathione peroxidase, glutathione peroxidase (GPx (glutathione peroxidase,), the early neurobehavioral development, the open field behavior of rats and the spatial memory ability of Morris water maze at different time points of 4 days and 7 days and 14 days after birth were studied. And by detecting the morphological development of brain nerve cells, The expression of (nestin), proliferating cell differentiation maturation protein (PCNA), glial fibrillary acidic protein (glial fibrillary acidic protein,GFAP), and 2Phosphate 3-cyclic nucleotide,3-phosphodiesterase,CNPase (2 ~ 3-cyclic nucleotide,3-phosphodiesterase,CNPase) in hippocampal neural progenitor cells (NPCs) were studied. Behavior, function to hippocampal local morphology and differentiation, mature protein expression, further in-depth study of selenium deficiency on the early neural development, to find the morphological structure and functional basis of this effect. Methods 1 the animal model of F344 low selenium rats was established according to the SD low selenium rat model which was successfully established by our group.
【學(xué)位授予單位】:汕頭大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2006
【分類號(hào)】:R363

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