本文選題：α-硫辛酸 + 視網(wǎng)膜�。� 參考：《遼寧醫(yī)學(xué)院》2011年碩士論文

【摘要】：目的 探討P53和Bax蛋白在大鼠視網(wǎng)膜缺血再灌注損傷中的表達(dá)以及α-硫辛酸對(duì)其表達(dá)的影響。 方法 選取正常無眼疾的SD大鼠72只,隨機(jī)分成正常組,視網(wǎng)膜缺血再灌注組(IR組)和α-硫辛酸干預(yù)組(LA+IR組)。然后根據(jù)再灌注時(shí)間的不同再將后兩組分成6 h,24 h,48 h,72 h組四個(gè)時(shí)間段。通過前房灌注升高眼壓的方法,制作大鼠視網(wǎng)膜缺血再灌注損傷(RIRI)的模型,光鏡觀察視網(wǎng)膜的組織形態(tài)學(xué)變化。采用Western blot法和SABC免疫組織化學(xué)法檢測(cè)在大鼠RIRI模型中P53、Bax蛋白的表達(dá)變化。 結(jié)果 正常組的大鼠視網(wǎng)膜組織結(jié)構(gòu)清晰完整,缺血再灌注組隨著再灌注時(shí)間的延長(zhǎng),視網(wǎng)膜的損害逐漸加重,內(nèi)層開始出現(xiàn)水腫、間質(zhì)逐漸萎縮變薄、層次不清,RGC層和內(nèi)核層細(xì)胞排列疏松而紊亂,并且減少。部分細(xì)胞出現(xiàn)核固縮、溶解、壞死、胞漿空泡樣變,72h以后視網(wǎng)膜結(jié)構(gòu)基本上恢復(fù)正常,整個(gè)視網(wǎng)膜變薄。說明視網(wǎng)膜結(jié)構(gòu)的損害呈進(jìn)行性、持續(xù)性、退行性。LA+IR組的組織學(xué)變化趨勢(shì)與IR組相似,但視網(wǎng)膜水腫、細(xì)胞丟失、核固縮及空泡樣變,均得到了一定程度的恢復(fù)。P53和Bax在正常視網(wǎng)膜組織中幾乎不表達(dá),在缺血再灌注6h開始表達(dá),24h達(dá)到高峰,48h開始下降,72h后發(fā)現(xiàn)表達(dá)明顯減弱。α-硫辛酸干預(yù)組,各觀察指標(biāo)的變化趨勢(shì)基本與缺血再灌注組相似,但表達(dá)明顯減弱,兩組間比較差異均有統(tǒng)計(jì)學(xué)意義(P0.05)。 結(jié)論 缺血再灌注過程主要對(duì)視網(wǎng)膜內(nèi)層造成損害,P53和Bax參與了視網(wǎng)膜缺血再灌注損傷的形成,α-硫辛酸可抑制視網(wǎng)膜組織中P53和Bax蛋白的表達(dá),對(duì)大鼠視網(wǎng)膜缺血再灌注損傷具有保護(hù)作用。
[Abstract]:Purpose To investigate the expression of p53 and Bax protein in rat retina ischemia reperfusion injury and the effect of 偽 -lipoic acid on the expression. Method Seventy-two normal SD rats without eye disease were randomly divided into normal group, retinal ischemia reperfusion group (IR group) and 偽 -lipoic acid intervention group (LA IR group). Then according to the different reperfusion time, the latter two groups were divided into six hours and 24 hours, 48 hours and 72 hours group. The rat model of retinal ischemia-reperfusion injury (RIRI) was established by anterior chamber perfusion to increase intraocular pressure (IOP). The histomorphologic changes of the retina were observed by light microscope. Western blot and SABC immunohistochemical methods were used to detect the expression of P53 and Bax protein in rat RIRI model. Result In the normal group, the retinal tissue structure was clear and complete. With the prolongation of reperfusion time, the damage of the retina was gradually aggravated, the inner layer began to appear edema, and the interstitial atrophy became thinner. The RGC layer and the nuclear layer were loosely arranged and disorganized, and decreased. Nuclear shrinkage, dissolution, necrosis occurred in some cells, and the retinal structure returned to normal after 72 hours of cytosolic vacuolar degeneration, and the whole retina became thinner. The histologic changes of the degenerative group were similar to those of the IR group, but the retinal edema, cell loss, nuclear pyknosis and vacuolar degeneration were observed. There was no expression of p53 and Bax in normal retina to some extent. The expression of P53 and Bax in normal retina was significantly decreased at the beginning of 6h after ischemia and reperfusion, and reached the peak at 24h and decreased at 48h. The expression of 偽 -lipoic acid was significantly decreased in the group treated with 偽 -lipoic acid. The change trend of the observed indexes was similar to that of the ischemia-reperfusion group, but the expression was obviously weakened, and the difference between the two groups was statistically significant (P 0.05). Conclusion Bax and p53 were involved in the formation of retinal ischemia-reperfusion injury. 偽 -lipoic acid inhibited the expression of p53 and Bax protein in retinal tissue. It has protective effect on retinal ischemia reperfusion injury in rats.
【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】：2011
【分類號(hào)】：R774.1

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