褪黑素对体外培养的人视网膜色素上皮细胞氧化损伤的保护作用

Objective To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. Methods The RPE cells were seeded and divided into normol control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1×10.7 mol/L,1×10-6 mol/L, 1×10-5 mol/L and 1×10-4 mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 μmol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic mothed, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. Results Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate(t=2.25,39.50,68.42;P<0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low M DA contents, and low apoptosis rate (P<0.05). Conclusions Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.     

人类视网膜色素上皮细胞体外培养的转分化

目的:研究人类视网膜色素上皮细胞(human retinal pig-ment epithelium,HRPE)体外培养的转分化现象。方法:倒置显微镜观察体外培养HRPE细胞形态变化;采用免疫细胞化学染色方法检测HRPE细胞角蛋白及α-平滑肌肌动蛋白(α-SMA)的变化。结果:HRPE细胞体外培养时形态由上皮细胞特征变化成为间质样细胞;细胞角蛋白表达与传代代数呈负相关(r=-0.831,P<0.001),α-SMA表达与传代代数呈正相关(r=0.456,P=0.002);角蛋白18表达高密度组较低密度组强(t=2.591,P=0.027);而α-SMA表达高密度组较低密度组弱(t=2.938,P=0.015)。结论:HRPE细胞体外培养转分化主要是体内外环境差异引起。     

褪黑素对体外培养的人视网膜色素上皮细胞氧化损伤的保护作用

目的 探讨褪黑素(Mel)对过氧化氢(H202)氧化损伤的人视网膜色素上皮(hRPE)细胞的保护作用及其作用机制.方法 实验研究.采用600μmoL/L H2O2建立体外培养的hRPE细胞氧化损伤模型.实验分为6组:溶剂对照组、600μmoL/L H2O2+溶剂组(H2O2损伤模型组)、600μmoL/L H2O2+10-7mol/L Mel组、600μmoL/L H2O2+10-6moL/L Mel组、600 μmol/L H2O2+10-5mol/L Mel组、600μmol/L H2O2+10-4moL/L Mel组.通过四甲基偶氮唑盐(MTT))法检测细胞活性;测定细胞内超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量以反映细胞氧化损伤程度;分别用DNA Ladders电泳法和流式细胞仪检测细胞的凋亡情况.溶剂对照组与600μmol/L H2O2组间均数比较采用随机区组设计的t检验;600μmol/L H2O2组以及600μmol/L H2O2+不同浓度Mel组间均数比较采用单因素5水平设计的方差分析,组间两两比较采用LSD-t检验.结果 H2O2模型组较对照组细胞活性明显降低、SOD活件降低、MDA含量增加、凋亡率升高,差异均有统计学意义(t=2.25,39.50,68.42;P<0.05);Mel干预组较模型组细胞活性升高、SOD活性升高、MDA含最减少、凋亡率降低,差异有统计学意义(P<0.05),并与药物浓度的变化呈正相关趋势.结论 Mel对H2O2诱导的RPE的氧化损伤具有保护作用,其机制可能与影响细胞活性、增强抗氧化酶活性、减少细胞凋亡有关.     

内蒙古地区单纯性病理性近视患者Decorin基因突变筛查

目的:研究内蒙古地区单纯性病理性近视患者核心蛋白聚糖(Decorin,DCN)基因与高度近视的关系.方法:收集单纯性病理性近视患者血液100例,视力正常者血液100例作为对照组,提取全血基因组DNA,应用聚合酶链反应(polymerase chain reaction,PCR)方法分别扩增DCN基因第7、第8个外显子及其邻近内含子并进行测序分析.统计学分析研究DCN基因外显子7、8的突变位点与单纯性病理性近视的相关性.结果:单纯性病理性近视患者100例中发现有2例发生突变,均为41775T→C,位于外显子8的邻近内含子区域,其余均未发现任何突变.与正常组对比差异无统计学意义(P＞0.05).结论:内蒙古地区单纯性病理性近视患者的DCN基因外显子7、8突变与本组高度近视无关.     

高度近视合并白内障植入Symfony与ZMB00 IOL视觉质量比较

目的：对比高度近视合并白内障患者植入tecnis Symfony人工晶状体(IOL)与tecnis ZMB00多焦点IOL的术后视觉质量。

方法：采用前瞻性非随机对照研究,纳入2020-06/2021-07在包头医学院第一附属医院行超声乳化吸除联合IOL植入术的高度近视合并白内障患者。依据患者所选IOL不同,分为Symfony组32例32眼和ZMB00组31例31眼。术后随访3mo,主要观察指标：比较术后1、3mo等效球镜,裸眼、最佳矫正远视力(5m),裸眼、最佳矫正远视力下中(80、60cm)、近(33cm)距离视力,术后3mo离焦曲线、对比敏感度、IOL偏心量及倾斜度。次要指标：术后3mo残余散光耐受度(90°、180°轴位,正、负柱镜)、视觉质量问卷。

结果：术后1、3mo两组裸眼、最佳矫正远视力、等效球镜比较均无差异(P>0.05),Symfony组裸眼、最佳矫正远视力下中视力优于ZMB00组,ZMB00组裸眼、最佳矫正远视力下近视力高于Symfony组(均P<0.05)。术后3mo Symfony组在+1.0～-3.0D跨度上,离焦曲线形成缓慢下降的平台期、视力优于0.3LogMAR,且在-1.0～-2.5D跨度上优于ZMB00组(均P<0.05); ZMB00组离焦曲线呈双峰状、在0、-3.00D上为波峰,-3.0～-3.5D跨度上优于Symfony组(P<0.05)。暗环境空间频率(3、6、12、18c/d)对比敏感度(CS),Symfony组优于ZMB00组(均P<0.05)。术后3mo两组IOL偏心量、倾斜度及视觉质量评分比较均无差异(P>0.05)。残余散光耐受度ZMB00组在+0.75D和-1.00D,Symfony组在+1.00D和-1.50D上表现出不适及视力低于0.3LogMAR(均P<0.05)。术后两组均不同程度出现眩光、光晕等不适,但随时间的推移症状大部分适应或消失。

结论：在高度近视合并白内障术后,两种IOL都有良好的囊袋稳定性及居中性,均能提供优秀的视觉质量。Symfony IOL可提供有效的连续视程、中视力更有优势、近视力表现略有不足,而ZMB00 IOL更适合对近距离视力有高要求者,Symfony IOL表现出更好的术后残余散光耐受度。     

LASIK术后主导眼对视功能影响的临床研究

目的:评价LASIK术前近视眼患者主导眼的分布及术后主导眼的变化与视力和视功能的关系。方法:选择拟行LASIK手术的近视眼患者235例470眼,分别于LASIK术前、术后1,3,6,12mo应用卡洞法行主导眼检查眼别,主导眼与非主导眼的术前的矫正视力和术后的视力进行比较,并接受视功能量表调查。结果:LASIK术前近视眼患者主导眼分布以右眼为主(67.2%);术前主导眼眼别与最佳矫正视力眼别一致性好,两者符合率为81.1%;235例近视患者LASIK术后主导眼眼别220例没有发生变化;15例患者眼别发生调换,其中5例有15°左右外斜。结论:主导眼分布以右眼为主,主导眼大多是患者最佳矫正视力眼;主导眼视力下降或低于非主导眼和主导眼调换患者在术后早期对视觉舒适度产生影响,但晚期影响降低患者逐渐适应。     

褪黑素对体外培养的人视网膜色素上皮细胞氧化损伤的保护作用

Objective To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. Methods The RPE cells were seeded and divided into normol control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1×10.7 mol/L,1×10-6 mol/L, 1×10-5 mol/L and 1×10-4 mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 μmol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic mothed, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. Results Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate(t=2.25,39.50,68.42;P<0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low M DA contents, and low apoptosis rate (P<0.05). Conclusions Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.     

褪黑素对体外培养的人视网膜色素上皮细胞氧化损伤的保护作用

Objective To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. Methods The RPE cells were seeded and divided into normol control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1×10.7 mol/L,1×10-6 mol/L, 1×10-5 mol/L and 1×10-4 mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 μmol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic mothed, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. Results Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate(t=2.25,39.50,68.42;P<0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low M DA contents, and low apoptosis rate (P<0.05). Conclusions Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.     

褪黑素对体外培养的人视网膜色素上皮细胞氧化损伤的保护作用

Objective To investigate the protective effects of melatonin on the retinal pigment epithelium (RPE) against oxidative damage induced by hydrogen dioxide (H2O2) and its mechanism. Methods The RPE cells were seeded and divided into normol control group, oxidative damage group and the treatment group (treated with melatonin at the concentration of 1×10.7 mol/L,1×10-6 mol/L, 1×10-5 mol/L and 1×10-4 mol/L). The model of oxidative damage on the RPE cells was established by culturing the RPE cells with H2O2 at the concentration of 600 μmol/L for 1 hour in vitro. The cell viability of RPE cells was detected by the methyl thiazolyl tetrazolium (MTT) method. The degree of oxidative damage was evaluated by detecting the superoxide dismutase (SOD) and maleic dialdehyde (MDA). Apoptosis was detected qualitatively using the DNA Ladders electrophoretic mothed, and quantitatively using the Annexin V-FITC/PI double staining flow cytometry. Results Compared with normal control group, the oxidative damage group had low cell viability, low SOD and high MDA contents, and high apoptosis rate(t=2.25,39.50,68.42;P<0.05). Compared with oxidative damage group, the treatment group had high cell viability, high SOD and low M DA contents, and low apoptosis rate (P<0.05). Conclusions Melatonin has a protective effect on the RPE against oxidative damage induced by H2O2. The mechanism may involve in reinforcing the cell viability, strengthening the activity of antioxidase, and reducing the apoptosis.     

病理性近视基因位点MYP3内基因的研究进展

近视是眼科最常见的疾病之一,病理性近视即近视度数≥-6.00D的近视,容易发生视网膜脱离,黄斑病变、视网膜周边格子样变性等并发症.MYP3基因是通过对混血常染色体显性遗传的单纯性病理性近视的大家系进行连锁分析和全基因组扫描分析发现的,并将MYP3基因定位于12q21～q23.而该区域内的基因Lumican、Decorin以及DSPG3被认为是最有可能引起高度近视的候选基因.本文将对MYP3内的高度近视候选基因进行论述.