重组人促红细胞生成素对大鼠视网膜缺血-再灌注损伤的保护作用

目的 制作Sprague-Dawley (SD)大鼠视网膜缺血-再灌注(RIR)损伤模型,探讨腹腔内注射重组人促红细胞生成素(rHuEPO)对急性RIR损伤所致的大鼠视网膜神经元损伤的保护作用及其对热休克蛋白72(HSP72)表达的影响.方法 采用前房灌注的方式建立RIR损伤模型,灌注压110 mm Hg(1 mm Hg=0.133kPa),缺血时间1h;腹腔注射rHuEPO.78只SD大鼠随机分组:正常组6只,EPO组、EPO+槲皮黄酮组、RIR组各24只,均以右眼为实验眼.采用免疫组织化学法和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)分别测定正常对照组和各实验组大鼠再灌注24h、48 h、72 h和1周视网膜中HSP72及凋亡细胞的表达,观察各组大鼠视网膜病理学改变.结果 ①正常组大鼠视网膜中HSP72表达微弱,各实验组大鼠视网膜中HSP72表达自再灌注12 h开始增强,24h达到高峰,随后逐渐减弱,72 h时表达稍高于正常.再灌注后各时间段,EPO组大鼠视网膜中HSP72表达均高于RIR组、EPO+槲皮黄酮组(P＜0.05).②正常大鼠视网膜中几乎没有凋亡细胞.再灌注后12 h,各实验组大鼠视网膜中可见凋亡细胞,24 h达高峰,48 h后凋亡细胞数逐渐减少;再灌注后各组大鼠视网膜中凋亡细胞数比正常组多(P＜0.05).③再灌注后,RIR组,EPO+槲皮黄酮组大鼠内层视网膜明显水肿,炎性细胞侵入,膜结构逐渐破坏;EPO组大鼠视网膜结构保持相对完整,炎性细胞相对较少.结论 ①HSP72在正常大鼠视网膜中表达微弱,RIR损伤后表达增多.腹腔注射EPO可以明显诱导大鼠视网膜中HSP72的表达增多.②EPO可以减少大鼠RIR损伤后视网膜细胞凋亡,减少视网膜内炎性细胞的浸润,保护视网膜结构,对视网膜具有明显的保护作用.其机制可能与使HSP72表达上调有关.(中国眼耳鼻喉科杂志,2012,12:30-35)     

雌激素对鼠视网膜缺血再灌注所致视网膜 损伤的保护作用

目的探讨雌激素对大鼠视网膜缺血再灌注所致视网膜损伤的保护作用。方法60只去势雌性SD大鼠随机分为2组，行前房灌注,建立视网膜缺血再灌注(RIR)模型。实验组在升高眼压前2 h按100 μg/kg的剂量皮下注射17β-雌二醇。对照组大鼠皮下注射等量生理盐水。分别在灌注前，再灌注后12、24、48、72 h对视网膜进行常规HE染色切片，观察细胞丢失情况及测量视网膜内层厚度。采用末端脱氧核酸转移酶介导的脱氧三磷酸尿苷缺口末端标记法（TUNEL法）检测视网膜组织中凋亡细胞的表达。结果实验组再灌注后24、48 h的凋亡细胞数目明显低于对照组(P<0.05),光学显微镜下计数视网膜神经节细胞数较对照组多(P<0.05)。结论雌激素对缺血再灌注所导致的视网膜损伤具有保护作用。(中华眼底病杂志,2005,21:177-179)     

大鼠视网膜组织缺血再灌注后视网膜内caspase-3的表达及意义

目的 在视网膜缺血再灌注模型上,观察再灌注后视网膜内caspase-3的动态变化,探讨caspase-3与视网膜细胞凋亡的关系.方法 结扎大鼠左侧颈总动脉1 h,然后再灌注,检测再灌注后1、6、12、24、48、72 h大鼠视网膜内caspase-3的水平及视网膜细胞凋亡平均发生率.结果 再灌注后视网膜内caspase-3的表达出现在光感受器细胞层,在再灌注后1、6、12、24、48、72 h caspase-3平均光密度分别为0.067±0.004、0.923±0.045、1.962±0.377、3.793±0.860、2.039±0.427、1.332±0.109,细胞凋亡平均发生率(%)分别为1.8±0.1,7.1±0.2,18.2±1.4,34.7±2.1,22.6±0.9,16.3±0.4.结论 再灌注后大鼠视网膜caspase-3表达与细胞凋亡呈现正相关,caspase-3可以促进视网膜细胞凋亡的发生.(中国眼耳鼻喉科杂志,2006,6347～349)     

果糖二磷酸镁对大鼠视网膜缺血再灌注损伤的保护作用

目的 探讨果糖二磷酸镁(magnesium fructose diphosphata,FDPMg)时实验性大鼠视网膜缺血再灌注损伤的影响及其作用机制.方法 通过升高眼压的方法,制作大鼠实验性视网膜缺血再灌注损伤的模型.将66只SD大鼠随机分为正常组、缺血再灌注模型组、FDPMg干预组.后两组各分为6 h、12 h、24 h、48 h、72 h 5个时间段.采用DNA原位末端标记法检测凋亡的视网膜细胞;免疫组织化学法检测视网膜组织中Fas/FasL蛋白的表达变化.结果 正常组大鼠视网膜未见凋亡细胞.缺血再灌注模型组再灌注6 h可观察到凋亡细胞;12 h凋亡细胞逐渐增加;24 h细胞凋亡达高峰;48 h凋亡细胞减少;72 h视网膜仍可见凋亡细胞.各组Fas/FasL表达情况与视网膜细胞凋亡情况基本一致.FDPMg干预组各时段各观察指标表达均较缺血再灌注模型组明显下降,两组间比较差异均有显著统计学意义(均为P＜0.01).结论 FDPMg明显抑制Fas/FasL蛋白在视网膜缺血再灌注损伤中的表达,进而抑制细胞凋亡来实现其对视网膜缺血再灌注损伤的保护作用.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

碱性成纤维细胞生长因子对视网膜缺血再灌注 损伤中凋亡相关基因表达的影响

目的探讨碱性成纤维细胞生长因子（bFGF）对视网膜缺血再灌注损伤（RIRI）中凋亡相关基因表达的影响。方法将28只Wistar大鼠随机分为正常组、缺血组和治疗组，其中后两组又按照不同再灌注时间分为再灌注后1、6、12、24、48、72 h 6个时间段。建立RIRI动物模型，以bFGF(治疗组)或平衡盐溶液（缺血组）玻璃体腔注射，通过免疫组织化学链酶卵白素 生物素复合体法检测不同时段视网膜组织中野生型（WT）p53、c-fos、c-jun基因的表达变化。结果缺血组视网膜再灌注后6 h可发现有WTp53、c-fos和c-jun蛋白的表达，24 h达到高峰，48 h仍持续强表达，72 h表达已明显下降。bFGF治疗组各观察指标变化规律基本与缺血组相似，但表达量相对明显减弱。二组比较，在再灌注6～48 h各时段差异有统计学意义（P＜0.05）。结论RIRI能引起WTp53、c-fos、c-jun基因在视网膜神经节细胞层与内核层表达的增高；WTp53、c-fos、c-jun基因可能通过在与RIRI的细胞凋亡中起作用而参与了RIRI的发生机制；bFGF可以抑制RIRI时WTp53、c-fos、c-jun基因在视网膜表达的增高,从而对RIRI起治疗作用。(中华眼底病杂志,2005,21:310-313)     

腺病毒载体介导的色素上皮衍生因子对大鼠视网膜缺血再灌注损伤的保护作用

目的:观察重组腺病毒介导的色素上皮衍生因子(Ad-PEDF)对大鼠视网膜缺血再灌注损伤的保护作用及机制。方法:选用健康大鼠96只,随机分为正常组、缺血再灌注组、缺血再灌注+Ad-CMV组,缺血再灌注+Ad-PEDF组,以前房加压的方法制备大鼠视网膜缺血再灌注模型,缺血再灌注+Ad-CMV组,缺血再灌注+Ad-PEDF组分别玻璃体腔注射Ad-CMV或Ad-PEDF1μL(滴度3.8×109/PFU),每组按照时间点12,24,72,168h,为4亚组,光学显微镜观察视网膜组织切片情况,并测量视网膜内层厚度及神经节细胞层神经节细胞数量。以TUNEL方法观察大鼠视网膜神经节细胞凋亡情况。结果:Ad-PEDF组视网膜内层厚度均超过缺血组及缺血+Ad-CMV组,Ad-PEDF组神经节细胞数目多于缺血组及Ad-CMV组,Ad-PEDF组视网膜神经节细胞凋亡细胞少于缺血组及Ad-CMV组,凋亡程度减轻,上述差异均具有显著性(P<0.05)。结论:腺病毒介导的色素上皮衍生因子玻璃体腔注射能够恢复大鼠视网膜缺血再灌注损伤所致的视网膜内层厚度降低,神经节细胞密度减少,具有保护作用。     

EPO对视网膜缺血再灌注损伤中WTp53、CyclinD1含量变化的影响

目的 研究促红细胞生成素(erythropoietin,EPO)与视网膜缺血再灌注损伤(retinal ischemical reperfusion injury,RIRI)视网膜组织中野生型p53(wild type p53,WTp53)、CyclinDl的关系,为EPO治疗RIRI提供理论依据.方法 前房穿刺加压法制作大鼠RIRI模型,28只大鼠随机分为正常组和手术组,其中手术组大鼠左眼为RIRI组,右眼为治疗组(于再灌注开始即刻玻璃体腔内注射EPO 20 IU),手术组又按照再灌注后不同时间段分为1h、6h、12h、24h、48h、72h组.SABC免疫组织化学法检测视网膜组织中WTp53、CyclinD1的表达.结果 RIRI组视网膜在再灌注6h后可发现有WTp3、CyclinD1的表达,24h达到高峰,48h仍持续强表达,72h表达已明显下降.玻璃体腔内注射EPO后上述因子表达趋势不变,但各时间点治疗组较RIRI组表达强度明显减少(P＜0.01).结论 玻璃体腔内注射EPO可以抑制WTp53、CyclinD1表达,这可能是EPO治疗RIRI的机制之一.     

Fas/FasL在视网膜缺血再灌注损伤中的表达与细胞凋亡的关系及碱性成纤维细胞生长因子的治疗作用

目的 探讨Fas/FasL在大鼠视网膜缺血再灌注损伤中的表达与细胞凋亡的关系及碱性成纤维细胞生长因子（basic fibroblast growth factor bFGF）的治疗作用。 方法 前房加压法制作大鼠视网膜缺血再灌注损伤模型，28只大鼠随机分为正常组和手术组，其中手术组大鼠左眼为缺血再灌注组，右眼为治疗组（玻璃体腔内注射bFGF），手术组又按照再灌注后不同时间段分为1、6、12、24、48、72 h组。应用末端脱氧核酸转移酶介导的脱氧三磷酸尿苷缺口末端标记（terminal deoxynucleotidyl transferase-mediated dUTP-biotinnick-end，TUNEL）法检测视网膜神经细胞凋亡指数(apoptosis index,AI)，免疫组织化学法检测视网膜组织中Fas、FasL的表达。 结果 视网膜神经细胞的凋亡出现于再灌注后6 h，并逐渐递增，24 h达到高峰，48 h开始下降，72 h组不明显。Fas、FasL 表达改变与凋亡的神经细胞改变基本一致。bFGF治疗组各观察指标表达变化规律与缺血组基本一致，但AI值在12、24、48 h组明显低于缺血组（P＜0.05）；Fas表达在6、12、24 h组较缺血组显著下降（P＜0.05）；FasL表达在12、24、48 h组较缺血组明显下降（P＜0.05）。 结论 Fas/FasL死亡诱导系统参与视网膜缺血再灌注损伤，导致神经节细胞的凋亡；bFGF可抑制Fas 、FasL的表达，减少神经节细胞凋亡，对视网膜缺血再灌注损伤有治疗作用。 （中华眼底病杂志，2003，19：160-163）     

大鼠视网膜缺血-再灌注损伤超微结构观察及机制探讨

目的研究大鼠视网膜缺血-再灌注损伤中的超微结构改变以及凋亡相关基因表达的变化,探讨其损伤机制。方法将28只大鼠随机分为正常组和手术组,手术组按照再灌注后不同时间段分为1h、6h、12h、24h、48h、72h组。前房加压法制作大鼠视网膜缺血-再灌注损伤模型,透射电镜检测视网膜超微结构改变,免疫组织化学法检测视网膜组织中bcl-2、bax、Fas的表达。结果(1)正常组视网膜神经纤维中微管及线粒体清晰可见;视网膜神经节细胞(retinal ganglion cells,RGCs)核大,电子密度低,核仁明显,细胞器丰富;再灌注损伤后RGCs核膜肿胀,线粒体嵴模糊不清,可见凋亡小体,神经纤维中微管模糊、减少甚至消失,以再灌注后24h为甚;(2)再灌注后6h,bax表达逐渐递增,24h达到高峰,48h开始下降,72h不明显;(3)bcl-2在视网膜神经节细胞层、纤维层及内核层有微弱表达,各个时间段变化不明显;(4)Fas表达改变与bax基本一致。结论视网膜缺血-再灌注损伤中,细胞凋亡是引起视网膜内核层和神经节细胞层细胞死亡的主要方式,其损伤机制与凋亡相关基因bcl-2、bax、Fas的表达变化有关。     

视网膜缺血再灌注损伤后视网膜神经节细胞pax6的表达变化与意义

【摘要】 目的 探索视网膜缺血再灌注损伤后视网膜神经节细胞pax6的表达变化及意义。 设计 实验研究。研究对象 缺血再灌注损伤大鼠视网膜。方法 成年健康雄性Sprague-Dawley大鼠 30只,随机选取5只作为空白对照组,其余25只为视网膜缺血再灌注损伤组,采用升高右眼眼压的 方法制作视网膜缺血再灌注损伤模型。视网膜缺血再灌注后1、2、4、6、8周分5组,每组5只,不 同时间点取右眼行免疫荧光染色,观察视网膜神经节细胞中pax6表达情况。主要指标 pax6的表达 。结果 视网膜缺血再灌注损伤后随着时间推移视网膜各层逐渐出现pax6表达阳性的细胞,对照组 视网膜神经节细胞pax6表达阳性率为（1.28±1.41）%,损伤后1、2、4、6、8周分别为（0.99± 1.23）%、（14.45±2.72）%、（50.88±4.73）%、（71.00±4.72）%、（78.80±4.62）% （F=1.350,P＜0.0001）。各组与对照组两两比较,缺血后1周视网膜神经节细胞pax6表达阳性率 差异无统计学意义（P=0.835）,缺血再灌注损伤2、4、6、8周视网膜神经节细胞pax6表达阳性率 均明显升高（P均＜0.0001）。结论 视网膜缺血再灌注损伤后视网膜各层均出现pax6表达阳性细胞 ,视网膜缺血再灌注损伤能诱导视网膜内源性干细胞激活。（眼科, 2012, 21： 414-417）     

促红细胞生成素对大鼠急性缺血视网膜节细胞的保护作用

目的:探讨重组人促红细胞生成素(recombinant human erythropoietin,rhEPO)对大鼠视网膜缺血再灌注损伤(retina ischemia reperfusion injury,RIR)中视网膜神经节细胞(retinal ganglion cell,RGC)的保护作用。方法:成年雌性SD大鼠20只,采用夹闭视网膜动脉30min造成大鼠双眼缺血再灌注模型。所有大鼠均于建模前1h给予左眼rhEPO10U(6μL),右眼给予同等剂量眼用平衡盐液。按照建模后眼球取材时间不同(1,4,7,14d)分为4组,每组5只,均于取材前4d利用荧光金(fluorogold,FG)逆行标记大鼠RGC,视网膜铺片RGC计数,比较双眼存活RGC数量。结果:rhEPO治疗眼RGC存活数多于平衡盐液对照眼。结论:rhEPO对大鼠视网膜急性缺血后RGC具有保护作用。     

视网膜缺血再灌注损伤中WTp53蛋白、CyclinD1表达的研究及bFGF对其的影响

目的探讨碱性成纤维细胞生长因子(bFGF)在大鼠视网膜缺血再灌注损伤(RIRI)中的治疗作用及机制。方法将28只Wistar大鼠随机分为正常组、缺血组和bFGF治疗组,其中后两组又按再灌注时间不同分为再灌注后1、6、12、24、48和72h6个时间段。通过前房穿刺加压法制作成RIRI动物模型,并在以bFGF(治疗组)或平衡盐溶液(缺血组)玻璃体腔注射后按不同时段处死动物,通过免疫组织化学链酶卵白素-生物素复合体(SABC)法检测各时段视网膜组织中野生型p53蛋白(WTp53)和细胞周期蛋白D1(CyclinD1)的表达变化。结果缺血组视网膜在再灌注后6h可发现有WTp53蛋白及CyclinD1的表达,24h达到高峰,48h仍持续强表达,72h表达已明显下降;bFGF治疗组各观察指标变化规律基本与缺血组相似,但表达量相对明显减弱,两组比较,在再灌注6-48h时段差别P值均<0.05,具有统计学意义。结论bFGF可抑制RIRI时WTp53蛋白和CyclinD1在视网膜表达的增高。