本文選題：苯甲酸雌二醇　切入點(diǎn)：缺血再灌注　出處：《遼寧醫(yī)學(xué)院》2012年碩士論文　論文類型：學(xué)位論文

【摘要】：目的 探討外源性雌激素對(duì)大鼠視網(wǎng)膜缺血再灌注損傷的保護(hù)作用機(jī)制及對(duì)Bcl-2和Caspase-3蛋白表達(dá)的影響。 方法 取72只雄性SD大鼠隨機(jī)分為正常組（N），單純?nèi)毖俟嘧⒔M（IR），苯甲酸雌二醇處理組(E2+IR)。其中后兩組又分別分為再灌注后6h、24h、48h，72h組（每組8只）。通過(guò)升壓裝置增加大鼠前房壓力建立大鼠視網(wǎng)膜缺血再灌注模型。對(duì)視網(wǎng)膜進(jìn)行常規(guī)HE染色光學(xué)顯微鏡下觀察視網(wǎng)膜組織形態(tài)變化，用免疫組織化學(xué)方法檢測(cè)視網(wǎng)膜組織中bcl-2、caspase-3蛋白的表達(dá)變化情況，采用DNA原位末端標(biāo)記（TUNEL）法檢測(cè)視網(wǎng)膜組織中的調(diào)亡細(xì)胞。 結(jié)果 正常組大鼠視網(wǎng)膜組織，層次分明；缺血再灌注組6h時(shí)視網(wǎng)膜組織各層出現(xiàn)不同程度的水腫，神經(jīng)節(jié)細(xì)胞層未見(jiàn)明顯空泡樣變性，內(nèi)外核層細(xì)胞排列變得輕度疏松、雜亂；內(nèi)外叢狀層也可見(jiàn)輕度水腫；24h視網(wǎng)膜組織高度水腫，神經(jīng)節(jié)細(xì)胞丟失嚴(yán)重，空泡樣變性明顯；內(nèi)外核層細(xì)胞排列變得雜亂；內(nèi)外叢狀層增厚明顯；48h后視網(wǎng)膜組織損害開(kāi)始有所好轉(zhuǎn)，72h時(shí)已經(jīng)基本恢復(fù)正常形態(tài)，但整個(gè)視網(wǎng)膜組織已變薄。而苯甲酸雌二醇處理組，視網(wǎng)膜組織形態(tài)變化趨勢(shì)與單純?nèi)毖俟嘧⒔M相似，但視網(wǎng)膜組織損害程度在各時(shí)點(diǎn)較單純?nèi)毖俟嘧⒔M有所好轉(zhuǎn)，整個(gè)視網(wǎng)膜也較正常薄。正常組大鼠視網(wǎng)膜組織幾乎無(wú)bcl-2、caspase-3蛋白的表達(dá)；單純?nèi)毖俟嘧⒔Mbcl-2和caspase-3蛋白在6h時(shí)已經(jīng)開(kāi)始表達(dá)，24h達(dá)高峰，48h表達(dá)開(kāi)始下降，72h仍有部分表達(dá)；而苯甲酸雌二醇處理組caspase-3蛋白的表達(dá)在各時(shí)間點(diǎn)上較單純?cè)俟嘧⒔M明顯下調(diào)（P㩳0.01）；Bcl-2蛋白的表達(dá)在各時(shí)間點(diǎn)上較單純?cè)俟嘧⒔M明顯上調(diào)（P㩳0.01）；兩組間比較均有統(tǒng)計(jì)學(xué)意義。正常視網(wǎng)膜組織幾乎未見(jiàn)凋亡細(xì)胞的表達(dá)，在IR組，隨時(shí)間的推移可見(jiàn)凋亡細(xì)胞增多，24h達(dá)高峰，48h有所減少；在E2+IR組，凋亡細(xì)胞表達(dá)的趨勢(shì)同IR組但在各時(shí)間點(diǎn)上的表達(dá)均比IR組有所減少，兩組比較均有統(tǒng)計(jì)學(xué)意義（P㩳0.01）。 結(jié)論 缺血再灌注損傷損害了視網(wǎng)膜組織結(jié)構(gòu)，導(dǎo)致了大量凋亡細(xì)胞的產(chǎn)生。Bcl-2、Caspase-3參與了視網(wǎng)膜缺血再灌注損傷中細(xì)胞凋亡的調(diào)控，苯甲酸雌二醇可上調(diào)Bcl-2蛋白的表達(dá)下調(diào)caspase-3蛋白的表達(dá)，而抑制細(xì)胞調(diào)亡，，保護(hù)視網(wǎng)膜組織。
[Abstract]:Purpose. To investigate the protective mechanism of exogenous estrogen on retinal ischemia reperfusion injury in rats and the effect of exogenous estrogen on the expression of Bcl-2 and Caspase-3 protein. Method. Seventy-two male SD rats were randomly divided into normal group, ischemia reperfusion group, estradiol benzoate treatment group and estradiol benzoate treatment group. The retinal ischemia-reperfusion model of rats was established by atrial pressure. The retinal tissue morphology was observed under the optical microscope with routine HE staining. Immunohistochemical method was used to detect the expression of bcl-2caspase-3 protein in retinal tissue, and DNA in situ end labeling (Tunel) method was used to detect the apoptotic cells in retinal tissue. Results. In the normal group, there were different degrees of edema in each layer of the retina at 6 h after ischemia reperfusion, no vacuolar degeneration was found in the ganglion cell layer, and the arrangement of the cells in the inner and outer nuclear layer became slightly loose and chaotic. Mild edema was also seen in the inner and outer plexiform layer. The retinal tissue was highly edematous, the ganglion cells were lost seriously, vacuolar degeneration was obvious, and the cells of the inner and outer nuclear layer were disordered. After 48 hours of thickening of the inner and outer plexiform layer, the damage of retinal tissue began to improve, but the whole retinal tissue was thinned after 72 hours, while in the group treated with estradiol benzoate, The morphologic changes of retinal tissue were similar to those of simple ischemia-reperfusion group, but the degree of retinal tissue damage was improved at each time point compared with that of simple ischemia-reperfusion group. The whole retina was thinner than normal. There was almost no expression of bcl-2ncaspase-3 in normal rat retina, but the expression of bcl-2 and caspase-3 in ischemia reperfusion group began to peak at 6h and decreased at 48h. The expression of caspase-3 protein in estradiol benzoate treated group was significantly lower than that in reperfusion group at all time points. The expression of Bcl-2 protein was significantly up-regulated at each time point compared with that of reperfusion group. There was no apoptotic cell expression in normal retinal tissue, but in IR group, the number of apoptotic cells increased to a peak at 24 h and decreased at 48 h in IR group, while in E 2 IR group, the number of apoptotic cells increased to a peak at 24 h and decreased at 48 h. The expression trend of apoptotic cells was similar to that of IR group, but the expression of apoptotic cells in IR group was lower than that in IR group at each time point, and there was statistical significance between the two groups. 0.01g. Conclusion. Ischemia-reperfusion injury damaged the structure of retinal tissue and resulted in the production of a large number of apoptotic cells. Bcl-2Caspase-3 was involved in the regulation of apoptosis in retinal ischemia-reperfusion injury. Estradiol benzoate up-regulated the expression of Bcl-2 protein and down-regulated the expression of caspase-3 protein, inhibited cell apoptosis and protected retinal tissue.
【學(xué)位授予單位】：遼寧醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R774.1

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