普罗布考预处理对大鼠视网膜缺血再灌注损伤的保护作用
发布时间：2018-10-17 09:09
【摘要】：目的探讨普罗布考预处理对视网膜缺血再灌注(retina ischemia reperfusion, RIR)损伤的保护作用及机制。 方法成年雄性无眼疾的wistar大鼠随机分成正常对照组,缺血对照组和预处理组。所有大鼠普通饲料喂养2周,正常对照组和缺血对照组按5m1/Kg体重予生理盐水灌胃2次／天,预处理组按5m1/Kg体重予普罗布考混悬液灌胃2次／天。缺血对照组和预处理组大鼠右眼前房灌注生理盐水形成14.3KPa高眼压,缺血60分后恢复血流,建立RIR损伤模型。分别于再灌注后1h、6h、12h、24h.48H、72h颈椎脱臼法随机处死缺血对照组和预处理组大鼠各10只,制备视网膜组织切片和视网膜组织匀浆。光学显微镜下观察视网膜组织学变化,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)原位检测视网膜神经元细胞的凋亡情况,分光光度法测定视网膜组织MDA含量及SOD活性水平。 结果(1)大鼠视网膜缺血再灌注后早期视网膜内层水肿增厚,晚期视网膜内层萎缩变薄；预处理组同缺血对照组比较,缺血再灌注早期水肿较轻,晚期视网膜内层萎缩程度轻(P0.05)。(2)正常对照组视网膜中凋亡细胞少见；缺血再灌注后6h开始有凋亡细胞阳性表达,24h凋亡细胞阳性表达达顶峰；预处理组细胞凋亡改变出现同缺血对照组相似的趋势j再灌注6h后各期凋亡阳性细胞数明显少于缺血对照组(P0.05)。(3)大鼠视网膜缺血再灌注后,缺血对照组视网膜内MDA含量逐渐上升,再灌注6h后含量较正常对照组高(P0.05)；预处理组视网膜MDA含量变化趋势同缺血对照组,再灌注6h后各时间点视网膜MDA含量均较缺血对照组低(P0.05)。视网膜缺血再灌注后,缺血对照组视网膜内SOD活性水平逐渐下降,6h后活性水平明显低于正常对照组(P0.01)；预处理组再灌注后SOD活性水平高于缺血对照组,再灌注后1h、6h、12h、24h比较有明显差异(P0.05)。 结论普罗布考预处理能够减轻大鼠视网膜缺血再灌注损伤,其保护机制可能与其能够减少缺血再灌注后神经元的凋亡,提高视网膜组织抗氧化能力,降低视网膜组织脂质过氧化物的形成有关。
[Abstract]:Objective to investigate the protective effect and mechanism of probucol preconditioning on retinal ischemia reperfusion (retina ischemia reperfusion, RIR) injury. Methods Adult male wistar rats without eye disease were randomly divided into normal control group, ischemic control group and preconditioning group. All rats were fed with normal diet for 2 weeks, the normal control group and ischemic control group were given normal saline twice a day according to 5m1/Kg body weight, and the pretreatment group received probucol suspension twice a day according to 5m1/Kg body weight. Rats in ischemic control group and preconditioning group were perfused with normal saline in right anterior chamber to form high intraocular pressure (IOP) and recovered blood flow after ischemia for 60 minutes to establish RIR injury model. One hour after reperfusion, 10 rats in the ischemic control group and 10 rats in the preconditioning group were randomly killed at 12 h, 24 h, 48 h and 72 h after reperfusion to prepare retinal tissue sections and retinal homogenate. The histological changes of retina were observed under optical microscope. The apoptosis of retinal neurons was detected by deoxyribonucleotide terminal transferase-mediated Nick end labeling (TUNEL) in situ. The content of MDA and the activity of SOD in retina were measured by spectrophotometry. Results (1) the edema of the inner layer of retina was thickened at the early stage and the inner layer of the retina shrank in the late stage after ischemia reperfusion in rats, and the edema in the preconditioning group was lighter than that in the ischemic control group. The degree of late retinal inner layer atrophy was light (P0.05). (2) the apoptotic cells were rare in normal control group, the positive expression of apoptotic cells began 6 hours after ischemia and reperfusion, and the positive expression of apoptotic cells reached the peak at 24 h after reperfusion. The changes of apoptosis in preconditioning group were similar to those in ischemic control group. The number of apoptotic positive cells in each phase of preconditioning group was significantly lower than that in ischemic control group (P0.05). (3). The content of MDA in retina of ischemic control group increased gradually. The content of retinal MDA in preconditioning group was the same as that in ischemic control group after 6 h reperfusion (P0.05), and the MDA content in retina of preconditioning group was lower than that of ischemic control group at 6 h after reperfusion (P0.05). The level of SOD activity in the retina of the ischemic control group decreased gradually after ischemia reperfusion, and was significantly lower than that in the normal control group after 6 hours (P0.01), and the activity level of SOD in the preconditioning group was higher than that in the ischemic control group after reperfusion. There was a significant difference (P 0.05) between 12 h and 12 h after reperfusion (P 0.05). Conclusion Probucol preconditioning can reduce retinal ischemia-reperfusion injury in rats, and its protective mechanism may be similar to that of probucol preconditioning to reduce neuronal apoptosis and increase the antioxidant capacity of retinal tissue after ischemia-reperfusion. It is related to reducing the formation of lipid peroxide in retina.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R774.1
本文编号：2276185
[Abstract]:Objective to investigate the protective effect and mechanism of probucol preconditioning on retinal ischemia reperfusion (retina ischemia reperfusion, RIR) injury. Methods Adult male wistar rats without eye disease were randomly divided into normal control group, ischemic control group and preconditioning group. All rats were fed with normal diet for 2 weeks, the normal control group and ischemic control group were given normal saline twice a day according to 5m1/Kg body weight, and the pretreatment group received probucol suspension twice a day according to 5m1/Kg body weight. Rats in ischemic control group and preconditioning group were perfused with normal saline in right anterior chamber to form high intraocular pressure (IOP) and recovered blood flow after ischemia for 60 minutes to establish RIR injury model. One hour after reperfusion, 10 rats in the ischemic control group and 10 rats in the preconditioning group were randomly killed at 12 h, 24 h, 48 h and 72 h after reperfusion to prepare retinal tissue sections and retinal homogenate. The histological changes of retina were observed under optical microscope. The apoptosis of retinal neurons was detected by deoxyribonucleotide terminal transferase-mediated Nick end labeling (TUNEL) in situ. The content of MDA and the activity of SOD in retina were measured by spectrophotometry. Results (1) the edema of the inner layer of retina was thickened at the early stage and the inner layer of the retina shrank in the late stage after ischemia reperfusion in rats, and the edema in the preconditioning group was lighter than that in the ischemic control group. The degree of late retinal inner layer atrophy was light (P0.05). (2) the apoptotic cells were rare in normal control group, the positive expression of apoptotic cells began 6 hours after ischemia and reperfusion, and the positive expression of apoptotic cells reached the peak at 24 h after reperfusion. The changes of apoptosis in preconditioning group were similar to those in ischemic control group. The number of apoptotic positive cells in each phase of preconditioning group was significantly lower than that in ischemic control group (P0.05). (3). The content of MDA in retina of ischemic control group increased gradually. The content of retinal MDA in preconditioning group was the same as that in ischemic control group after 6 h reperfusion (P0.05), and the MDA content in retina of preconditioning group was lower than that of ischemic control group at 6 h after reperfusion (P0.05). The level of SOD activity in the retina of the ischemic control group decreased gradually after ischemia reperfusion, and was significantly lower than that in the normal control group after 6 hours (P0.01), and the activity level of SOD in the preconditioning group was higher than that in the ischemic control group after reperfusion. There was a significant difference (P 0.05) between 12 h and 12 h after reperfusion (P 0.05). Conclusion Probucol preconditioning can reduce retinal ischemia-reperfusion injury in rats, and its protective mechanism may be similar to that of probucol preconditioning to reduce neuronal apoptosis and increase the antioxidant capacity of retinal tissue after ischemia-reperfusion. It is related to reducing the formation of lipid peroxide in retina.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R774.1
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