α-硫辛酸对大鼠视网膜缺血再灌注损伤中P53、Bax表达的影响

发布时间：2018-05-16 00:36

本文选题：α-硫辛酸 + 视网膜　；参考：《辽宁医学院》2011年硕士论文

【摘要】：目的探讨P53和Bax蛋白在大鼠视网膜缺血再灌注损伤中的表达以及α-硫辛酸对其表达的影响。方法选取正常无眼疾的SD大鼠72只,随机分成正常组,视网膜缺血再灌注组(IR组)和α-硫辛酸干预组(LA+IR组)。然后根据再灌注时间的不同再将后两组分成6 h,24 h,48 h,72 h组四个时间段。通过前房灌注升高眼压的方法,制作大鼠视网膜缺血再灌注损伤(RIRI)的模型,光镜观察视网膜的组织形态学变化。采用Western blot法和SABC免疫组织化学法检测在大鼠RIRI模型中P53、Bax蛋白的表达变化。结果正常组的大鼠视网膜组织结构清晰完整,缺血再灌注组随着再灌注时间的延长,视网膜的损害逐渐加重,内层开始出现水肿、间质逐渐萎缩变薄、层次不清,RGC层和内核层细胞排列疏松而紊乱,并且减少。部分细胞出现核固缩、溶解、坏死、胞浆空泡样变,72h以后视网膜结构基本上恢复正常,整个视网膜变薄。说明视网膜结构的损害呈进行性、持续性、退行性。LA+IR组的组织学变化趋势与IR组相似,但视网膜水肿、细胞丢失、核固缩及空泡样变,均得到了一定程度的恢复。P53和Bax在正常视网膜组织中几乎不表达,在缺血再灌注6h开始表达,24h达到高峰,48h开始下降,72h后发现表达明显减弱。α-硫辛酸干预组,各观察指标的变化趋势基本与缺血再灌注组相似,但表达明显减弱,两组间比较差异均有统计学意义(P0.05)。结论缺血再灌注过程主要对视网膜内层造成损害,P53和Bax参与了视网膜缺血再灌注损伤的形成,α-硫辛酸可抑制视网膜组织中P53和Bax蛋白的表达,对大鼠视网膜缺血再灌注损伤具有保护作用。
[Abstract]:Purpose To investigate the expression of p53 and Bax protein in rat retina ischemia reperfusion injury and the effect of 伪 -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 伪 -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 伪 -lipoic acid was significantly decreased in the group treated with 伪 -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. 伪 -lipoic acid inhibited the expression of p53 and Bax protein in retinal tissue. It has protective effect on retinal ischemia reperfusion injury in rats.
【学位授予单位】：辽宁医学院
【学位级别】：硕士
【学位授予年份】：2011
【分类号】：R774.1

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