本文關(guān)鍵詞：組織激肽釋放酶8在宮內(nèi)生長(zhǎng)受限大鼠海馬中的表達(dá)及其意義　出處：《蘇州大學(xué)》2012年碩士論文　論文類型：學(xué)位論文

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【摘要】：目的：用孕期全程低蛋白（6%）飲食法制造宮內(nèi)生長(zhǎng)受限（Intrauterine growthretardation,IUGR）仔鼠腦損傷模型，觀察組織激肽釋放酶8（Neuropsin，KLK8）在海馬中的表達(dá)變化，檢測(cè)仔鼠學(xué)習(xí)記憶能力，探討IUGR發(fā)生腦損傷的機(jī)制。 方法：選取健康三月齡Sprague-Dawley大鼠28只，按照雌雄1：1的比例置于同一籠中交配。受孕成功的孕鼠隨機(jī)分為對(duì)照組和IUGR組。對(duì)照組母鼠自受孕后第一天開始給予21%正常蛋白飲食，而IUGR組母鼠自受孕后第一天開始給予6%低蛋白飲食，建立IUGR仔鼠模型。兩組仔鼠生后至21日的哺乳期內(nèi)，均給予母鼠21%正常蛋白飲食喂養(yǎng)、自由飲水。21日后將母鼠與仔鼠分籠，給予兩組仔鼠21%正常蛋白飲食喂養(yǎng)、自由飲水，喂養(yǎng)至32日。選擇1日、5日、10日和21日作為觀察的4個(gè)時(shí)間點(diǎn)，每個(gè)時(shí)間點(diǎn)每組有6只仔鼠，測(cè)量仔鼠體重、頭臀長(zhǎng)、腦濕重，并對(duì)各個(gè)時(shí)間點(diǎn)仔鼠留取海馬組織，HE染色觀察1日及21日海馬結(jié)構(gòu)的變化，用Westernblot檢測(cè)海馬組織中組織激肽釋放酶8的表達(dá)，于26日至32日行Morris水迷宮測(cè)試，檢測(cè)仔鼠學(xué)習(xí)記憶能力。 結(jié)果：1、兩組仔鼠體格生長(zhǎng)及腦重的動(dòng)態(tài)比較：與對(duì)照組相比，1日齡IUGR仔鼠形態(tài)瘦小，體重、頭臀長(zhǎng)及腦濕重均降低（P＜0.05）；5日齡及10日齡時(shí)體重、頭臀長(zhǎng)及腦濕重仍落后（P＜0.05）；經(jīng)追趕生長(zhǎng)，到21日齡時(shí)，體重、頭臀長(zhǎng)無明顯差異（P＞0.05），腦濕重仍低（P＜0.05）。 2、兩組仔鼠海馬HE染色的變化：與對(duì)照組相比，1日齡時(shí)IUGR仔鼠海馬神經(jīng)元細(xì)胞排列疏松、紊亂，細(xì)胞數(shù)目減少；部分細(xì)胞水腫明顯，出現(xiàn)空泡；核固縮細(xì)胞比較多，出現(xiàn)凋亡細(xì)胞。21日齡時(shí)IUGR組神經(jīng)元細(xì)胞水腫基本消失，但細(xì)胞排列仍相對(duì)疏松、紊亂，細(xì)胞數(shù)目未見明顯增多。 3、兩組仔鼠海馬中組織激肽釋放酶8的表達(dá)：在四個(gè)時(shí)間點(diǎn)，1日齡時(shí)兩組仔鼠組織激肽釋放酶8的表達(dá)低，5日齡時(shí)兩組仔鼠組織激肽釋放酶8的表達(dá)增加，10日齡和21日齡時(shí)兩組仔鼠組織激肽釋放酶8的表達(dá)急劇增加；與對(duì)照組相比，，在四個(gè)時(shí)間點(diǎn)， IUGR仔鼠組織激肽釋放酶8的表達(dá)均低于對(duì)照組（P＜0.05）。 4、Morris水迷宮實(shí)驗(yàn)顯示：（1）兩組仔鼠逃避潛伏期于測(cè)試第1天至第5天逐漸縮短；第5天IUGR組逃避潛伏期明顯長(zhǎng)于對(duì)照組，具有統(tǒng)計(jì)學(xué)意義（P0.05）。（2）搜尋策略結(jié)果：第5天時(shí)，IUGR組和對(duì)照組成績(jī)比較有差異，具有統(tǒng)計(jì)學(xué)意義（P0.05）。（3）兩組穿越平臺(tái)次數(shù)無明顯差異（P0.05）。 結(jié)論：1、用6%低蛋白飲食法能建立IUGR大鼠腦損傷模型。 2、IUGR仔鼠體態(tài)瘦小，腦重低，海馬神經(jīng)元細(xì)胞數(shù)目少。給予IUGR仔鼠正常喂養(yǎng)，體格上可實(shí)現(xiàn)追趕生長(zhǎng)，但腦重、神經(jīng)元數(shù)目仍落后于正常仔鼠，并且出現(xiàn)學(xué)習(xí)能力的降低。 3、IUGR仔鼠組織激肽釋放酶8在海馬中的表達(dá)量一直低于正常組仔鼠，組織激肽釋放酶8表達(dá)的下降可能是IUGR發(fā)生腦損傷的機(jī)制之一。
[Abstract]:Objective: to produce intrauterine growthretardation with intrauterine growth restriction (ICGR) by using a diet with low protein content during pregnancy. The brain injury model of IUGR-based rats was used to observe the expression of KLK8 in hippocampus and the ability of learning and memory. To explore the mechanism of brain injury in IUGR. Methods: 28 healthy three-month-old Sprague-Dawley rats were selected. The pregnant mice were randomly divided into control group and IUGR group according to the ratio of male and female 1: 1. The control group was given 21% normal protein diet from the first day after conception. In IUGR group, the female rats were given 6% low-protein diet from the first day after conception to establish the IUGR rat model. The two groups were breast-feeding from postnatal to 21st. All rats were fed with 21% normal protein diet. After free drinking, the rats were divided into cages and fed with 21% normal protein diet for 32 days. Choose 1st. Four time points were observed on 5th, 10th and 21st. There were 6 rats in each group at each time point. The body weight, length of head and hip, brain wet weight were measured, and hippocampal tissue was retained at each time point. The changes of hippocampal structure in 1st and 21st were observed by HE staining, and the expression of kallikrein 8 in hippocampus was detected by Westernblot. Morris water maze test was performed from 26th to 32 to test the learning and memory ability of young mice. Results compared with the control group, the body growth and brain weight of the two groups were compared with those of the control group. Compared with the control group, the body weight, body weight, head and hip length and brain wet weight of 1-day-old IUGR rats were decreased (P < 0.05). At 5 and 10 days of age, the body weight, the length of head and hip and the wet weight of brain still lagged behind (P < 0.05). At 21 days of age, there was no significant difference in body weight and length of head and hip (P > 0.05), and the brain wet weight was still low (P < 0.05). 2, the changes of HE staining in hippocampus of the two groups: compared with the control group, the hippocampal neurons of IUGR rats were loosely arranged, disordered and the number of cells decreased at 1 day old compared with the control group. Some of the cells showed obvious edema and vacuoles. There were many pyknotic cells in the nucleus. The edema of neurons in the IUGR group disappeared basically at the age of 21 days, but the arrangement of the cells was still relatively loose and disordered, and the number of the cells did not increase significantly. 3, the expression of kallikrein 8 in hippocampus of the two groups: the expression of kallikrein 8 was low at the age of 1 day at four time points. The expression of kallikrein 8 in the tissues of the two groups increased sharply at the age of 5 days and 21 days, respectively, and the expression of kallikrein 8 increased sharply at the age of 10 days and 21 days of age, and the expression of kallikrein 8 in the tissues of the two groups increased sharply. Compared with the control group, the expression of kallikrein 8 in the tissues of IUGR rats was lower than that of the control group at four time points (P < 0.05). (4) Morris water maze test showed that the escape latency of the two groups was shortened from the first day to the fifth day. On the 5th day, the escape latency of IUGR group was significantly longer than that of control group, with statistical significance (P 0.05). The result of search strategy: on the 5th day, there were differences between IUGR group and control group. There was no significant difference in the frequency of crossing the platform between the two groups. Conclusion the brain injury model of IUGR rats can be established by 6% low protein diet. 2IUGR mice were small in body, low in brain weight, and few in the number of hippocampal neurons. Given normal feeding to the IUGR offspring, they could catch up and grow physically, but the brain was heavy. The number of neurons still lagged behind that of normal mice, and the learning ability decreased. 3The expression of kallikrein 8 in hippocampus of pups with IUGR was lower than that of normal rats, and the decrease of expression of kallikrein 8 might be one of the mechanisms of brain injury in IUGR.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R341

【參考文獻(xiàn)】

相關(guān)期刊論文 前10條

1 柯志勇,劉軍,丘小汕;三種宮內(nèi)發(fā)育遲緩大鼠模型方法的比較[J];中國當(dāng)代兒科雜志;2000年01期

2 盧巖;劉曉梅;李書琴;;L-精氨酸對(duì)宮內(nèi)發(fā)育遲緩胎鼠胰島素樣生長(zhǎng)因子及其結(jié)合蛋白表達(dá)的影響[J];中國當(dāng)代兒科雜志;2006年04期

3 鮑娟;楊期東;;熱休克蛋白70在阿爾茨海默病中作用的研究進(jìn)展[J];國際神經(jīng)病學(xué)神經(jīng)外科學(xué)雜志;2008年03期

4 周雯慧,周春,張?jiān)?王燕;宮內(nèi)發(fā)育遲緩幼鼠NMDA受體表達(dá)異常和中樞神經(jīng)系統(tǒng)功能變化[J];武漢大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2004年04期

5 黃譜;茍文麗;蔣馬麗;張瑞;孫云萍;;胎兒生長(zhǎng)受限模型大鼠子代空間學(xué)習(xí)記憶能力改變的研究[J];四川大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2008年04期

6 林亞芬,李偉華,周海燕,濮澤瓊,陳碧琴,陳兆文;宮內(nèi)發(fā)育遲緩兒身長(zhǎng)、體重、頭圍的追趕比較[J];復(fù)旦學(xué)報(bào)(醫(yī)學(xué)版);2005年06期

7 婁江濤;胡成進(jìn);;組織型激肽釋放酶及相關(guān)肽酶在中樞神經(jīng)系統(tǒng)中的作用[J];生命的化學(xué);2010年02期

8 翁梅倩,張偉利,李紉秋;小于胎齡兒體格及智能發(fā)育的隨訪觀察[J];中國優(yōu)生優(yōu)育;1999年02期

9 杜艷;趙利華;吳海標(biāo);王進(jìn)聲;姚平;;艾炷灸對(duì)D-半乳糖衰老小鼠學(xué)習(xí)記憶能力和大腦皮質(zhì)、海馬區(qū)c-fos蛋白表達(dá)的影響[J];時(shí)珍國醫(yī)國藥;2011年01期

10 黃譜;茍文麗;米陽;張瑞;孫云萍;;胎兒生長(zhǎng)受限子代大鼠與正常大鼠海馬蛋白質(zhì)組雙向電泳圖譜比較[J];西安交通大學(xué)學(xué)報(bào)(醫(yī)學(xué)版);2009年05期

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