期刊文献+

N-乙酰-5-羟色胺(NAS)对视网膜缺血再灌注损伤(RIRI)大鼠视网膜活性Caspase-3、Bcl-2、Bax表达的影响 被引量:12

Effects of N-acetylserotonin on expression of active caspase-3,Bcl-2 and Bax protein in rat retina after ischemia-reperfusion injury
下载PDF
导出
摘要 目的探讨N-乙酰-5-羟色胺(N-acetylserotonin,NAS)对视网膜缺血再灌注损伤(retinal ischemia-reperfusion injury,RIRI)大鼠视网膜活性Caspase-3、Bcl-2、Bax表达的影响。方法取健康成年Sprague-Dawley大鼠66只,采用随机数字表法随机分为正常对照组(6只)、缺血再灌注组(30只)与药物组(30只),药物组于造模前30 min腹腔注射5 mg·kg-1NAS,缺血再灌注组腹腔注射同等剂量的生理盐水,缺血再灌注组与药物组按RIRI后时间,分为6 h、12 h、24 h、48 h、72 h五个亚组。采用HE染色法观察各组视网膜形态学变化,免疫组织化学染色检测各组大鼠视网膜活性Caspase-3、Bcl-2及Bax蛋白表达。结果HE染色显示正常对照组大鼠视网膜结构清晰,各层细胞排列紧密;缺血再灌注组大鼠RIRI后6 h、12 h视网膜各层高度水肿,24 h后水肿逐渐减轻,神经节细胞逐渐减少,分布较紊乱,随着时间延长,视网膜神经节细胞大片缺失;药物组6 h、12 h较缺血再灌注组细胞水肿明显减轻,24 h、48 h、72 h组较缺血再灌注组细胞排列规整,神经节细胞数量减少减轻。缺血再灌注组视网膜活性Caspase-3阳性细胞数在灌注后6 h开始表达增加,阳性细胞数为(561.15±37.19)个·mm^(-2),24 h达到较高水平,阳性细胞数为(1522.61±84.36)个·mm^(-2),随后逐渐下降,药物组视网膜各时间点活性Caspase-3阳性细胞数均显著少于缺血再灌注组,差异均有统计学意义(均为P<0.05)。正常对照组视网膜可见大量Bcl-2阳性细胞;缺血再灌注组RIRI后6 h Bcl-2阳性细胞开始下降,12 h后继续减少,24 h降至较低水平;药物组各时间点Bcl-2阳性细胞数均显著多于缺血再灌注组,差异均有统计学意义(均为P<0.05)。正常对照组大鼠视网膜几乎未见Bax阳性细胞;缺血再灌注组RIRI后6 h神经节细胞层及内核层可见Bax阳性细胞,24 h达到较高水平,48 h开始下降;药物组各时间点Bax阳性细胞均显著少于缺血再灌注组,差异均有� Objective To investigate the effects of N-acetylserotonin (NAS) on the expression of active caspase-3,Bcl-2 and Bax in rat retinas induced by retinal ischemia-reperfusion injury (RIRI).Methods Adult male Sprague- Dawley rats were randomly divided into the normal control group (6 cases),RIRI group (30 cases) and NAS group (30 cases),RIRI models in NAS group were established after giving NAS,the groups were sub-divided into 6 hours,12 hours,24 hours,48 hours and 72 hours group based on the time of RIRI.Morphologic changes were evaluated by HE staining.The expression of active caspase-3,Bcl-2 and Bax protein in the retina of rats was detected by immunohistochemistry.Results HE staining showed that the retinal structure in the normal control group was clear,and the cells in each layer were tightly packed;Each layer of retina was edema in the RIRI group after 6 hours and 12 hours,the edema gradually alleviated after 24 hours,the ganglion cells decreased gradually,the distribution was in disorder,with the prolongation of time,the retinal ganglion cells were defected;drug group of as Compared with RIRI group,the cell edema in the NAS group at 6 hours and 12 hours were obvious reduced,the cells in 24 hours,48 hours,72 hours group arranged regularly,the loss number of ganglion cells were reduced.The number of active caspase-3 positive cells in RIRI group increased at 6 hours after perfusion,the number was (561.15±37.19) cell·mm-2,and reached the high level at 24 hours,the number was (1522.61±84.36) cell·mm-2,and then decreased gradually.The number of active caspase-3 positive cells in NAS group was significantly lower than that in RIRI group,the difference was statistically significant (all P〈0.05).The expression of Bcl-2 positive cells in RIRI group began to decrease after 6 hours,and decreased to a low level at 24 hours,and the number of Bcl-2 positive cells in NAS group was significantly higher than that in RIRI group at each time point,the differences were statistically significan
出处 《眼科新进展》 CAS 北大核心 2017年第8期701-704,708,共5页 Recent Advances in Ophthalmology
基金 国家自然科学基金资助(编号:81000268) 山东省自然科学基金项目(编号:ZR2013HL067 ZR2014HQ077 ZR2014-JL049) 山东省医药卫生科技发展计划项目(编号:2013WS0295) 山东省高等学校科技计划项目(编号:J15LL08)~~
关键词 N-乙酰-5-羟色胺 视网膜缺血再灌注损伤 活性Caspase-3 BCL-2 BAX N-acetylserotonin retinal ischemia-reperfusion injury active caspase-3 Bcl-2 Bax
  • 相关文献

参考文献2

二级参考文献11

  • 1张跃红,牛膺筠,王红云,周占宇,刘成桂.低氧预适应对小鼠视网膜光感受器细胞光损伤的防护作用[J].中华眼科杂志,2005,41(7):631-635. 被引量:12
  • 2Mukaida Y,Machida S,Masuda T,Tazawa Y. Correlation of retinal function with retinal histopathology following ischemiareperfusion in rat eyes[J].Current Eye Research,2004,(06):381-389. 被引量:1
  • 3Qiu W,Wei R,Zhang C,Zhang C,Leng W,Wang W. A glycine site-specific NMDA receptor antagonist protects retina ganglion cells from ischemic injury by modulating apoptotic cascades[J].Journal of Cellular Physiology,2010,(03):819-826. 被引量:1
  • 4Liu J,Narasimhan P,Yu F,Chan PH. Neuroprotection by hypoxic preconditioning involves oxidative stress-mediated expression of hypoxia-inducible factor and erythropoietin[J].Stroke,2005,(06):1264-1269. 被引量:1
  • 5Shukla D,Saxena S,Jayamurthy P,Sairam M,Singh M,Jain SK. Hypoxic preconditioning with cobalt attenuates hypobaric hypoxia-induced oxidative damage in rat lungs[J].High Altitude Medicine & Biology,2009,(01):57-69. 被引量:1
  • 6Leconte C,Tixier E,Freret T,Toutain J,Saulnier R,Boulouard M. Delayed hypoxic postconditioning protects against cerebral ischemia in the mouse[J].Stroke,2009,(10):3349-3355. 被引量:1
  • 7Costa GN,Vindeirinho J,Cavadas C,Ambrósio AF,Santos PF. Contribution of TNF receptor 1 to retinal neural cell death induced by elevated glucose[J].Molecular and Cellular Neuroscience,2012,(01):113-123. 被引量:1
  • 8Niu YJ,Zhao YS,Gao YX,Zhou ZY Wang HY Yuan CY. Therapeutic effect of bFGF on retina ischemia-reperfusion injury[J].Chinese Medical Journal(Engl),2004,(02):252-257. 被引量:1
  • 9祝文文,曹永亮,王晓莉,赵岩松,范姗姗.MSC移植对缺血再灌注损伤视网膜神经节细胞Bcl-2/Bax表达的影响[J].眼科新进展,2011,31(5):404-406. 被引量:3
  • 10房澍名,李春生,安君艳,敦志娜,姚冬梅,刘蕾,张晓岚.细胞外信号调节激酶在丹参单体IH764-3诱导肝星状细胞凋亡中的作用[J].中国应用生理学杂志,2011,27(4):402-406. 被引量:8

共引文献15

同被引文献66

引证文献12

二级引证文献29

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部