自然光照对眼部的影响

自然光照由连续光谱、不同能量的光组成,光的波长越短能量越大,故其中紫外线和蓝光具有更高能量。暴露在高强度光照下可能导致眼部组织细胞损伤,进而引起各种眼部结构的病理变化。我们回顾了近年来有关光照在角结膜、晶状体、前房结构、视网膜、视神经相关疾病中的作用的研究,综述了光照在眼部可能触发的信号通路和作用机制。眼组织过度暴露在光照下会导致DNA损伤增加、蛋白质的异常修饰和聚集,以及过度的氧化应激,从而导致眼部疾病的发生发展。因此,可根据所接触的光照特性与强度,以及需要保护的眼组织类型,针对性地单独或联合使用物理保护、局部和/或口服抗氧化剂和光照活化信号通路的小分子抑制剂,以防止和减少光照引起的眼部损害。     

自然光暴露对PRK法单眼远视离焦幼年恒河猴角膜组织的影响

目的：探讨自然光暴露对单眼远视离焦幼年恒河猴正常和准分子激光角膜切削术(PRK)损伤后角膜组织潜在的光损伤作用。

方法：选取12只2月龄恒河猴,行右眼PRK,矫正度数为-4.0D,制作单眼远视离焦近视动物模型。幼猴体质量和性别均衡配对后分为两组：人工照明组(AL组,n=6)和自然光组(NL组,n=6)。两组幼猴饲养于同一人工照明条件室内饲养环境,NL组幼猴每天9：00～11：00和15：00～17：00于室外随单笼接受自然光照射。PRK术后裂隙灯检查比较两组PRK眼角膜愈合及haze形成情况; PRK术后50d,每组各取4只幼猴双眼泪液,采用蛋白质芯片法检测泪液11种细胞因子含量。PRK术后180d取角膜组织,分别行病理组织学检查组织结构变化; 免疫组织化学法检测TGF-β1和α-SMA表达; TUNEL法检测细胞凋亡以及采用羟胺法和硫代巴比妥酸法分别测定角膜上皮细胞SOD和MDA含量。

结果：PRK术后NL组PRK眼出现一过性haze,术后40d两组haze分级评估有差异(P=0.015)。PRK术后50d,两组PRK眼泪液EGF和TGF-β1含量均有差异(P=0.045、0.038),两组间对侧眼均无差异(P>0.05); 且AL组、NL组组内泪液TGF-β1水平有差异(P=0.003、0.036)。术后180d,两组双眼角膜组织形态学一致; 角膜组织内各层偶见细胞凋亡染色,且无明显TGF-β1和α-SMA表达; 两组PRK眼和对侧眼角膜上皮细胞SOD活力和MDA含量均无差异(P>0.05)。

结论：自然光照射量可加剧幼猴PRK术后角膜组织修复反应,但远期未对角膜组织造成不可逆病理组织学改变,对正常的幼猴角膜组织无明显光损伤作用。     

氢对氧化应激诱导的视网膜衰老的保护机制

目的：探讨氢对氧化应激诱导的视网膜衰老的保护机制。

方法：将小鼠随机分为三组：对照组、模型组(NaIO₃处理组)和治疗组(H₂水灌胃组)。模型组通过鼠尾静脉注射NaIO₃溶液建立视网膜氧化应激损伤模型; 对照组小鼠注射生理盐水; 治疗组予富含H₂的饮用水灌胃后造模。利用SA-β-gal染色检测视网膜衰老情况。收集小鼠视网膜,western-blot检测DNA损伤反应相关蛋白ATM、NF-κB蛋白、细胞周期蛋白D1(Cyclin D1)和DNA修复相关蛋白HMGB1的表达。

结果：SA-β-gal染色显示,治疗组蓝绿色沉淀较模型组相比减少。western-blot结果显示治疗组中DNA损伤反应相关蛋白ATM、NF-κB、Cyclin D1相对表达量(0.10±0.009、0.32±0.01、0.19±0.002)较模型组(0.77±0.08、0.70±0.02、0.36±0.01)均显著降低,差异均具有统计学意义(均P<0.01); 而治疗组中DNA修复相关蛋白HMGB1相对表达量(0.927±0.06)较模型组(0.383±0.07)显著升高,差异有统计学意义(P<0.01)。

结论：氢可以通过抑制氧化应激诱导的DNA损伤减弱视网膜衰老。     

视网膜光损伤机制的研究进展

视网膜是一种高度专业化的组织,具有独特的结构及适应性,在所有不同类型的视网膜细胞中保持动态平衡对于维持视力至关重要。视网膜可能会暴露在各种环境损伤中,如光诱导的损伤,在进化过程中,视网膜细胞对各种损伤产生了适应性反应,这些反应共同恢复了细胞的动态平衡,并增加了组织对进一步损伤的抵抗力。然而过度光照则会导致视网膜组织内光感受器细胞、视网膜神经节细胞(RGC)、视网膜神经胶质细胞及视网膜色素上皮细胞(RPE)发生一系列病理改变,包括线粒体内活性氧(ROS)和Ca²⁺浓度增加、细胞凋亡、内质网应激、细胞自噬和炎症等,从而导致视网膜发生不可逆损伤。本文将对视网膜光损伤的发病机制和相关研究进展进行详细阐述,为未来防治视网膜光损伤提供研究方向。     

The role of sunlight in human cataract formation

This review summarizes and integrates new findings concerning the role of near-ultraviolet radiation, as is present in sunlight and common artificial light sources, in stimulating human and animal cataract formation. Epidemiological and basic research studies are summarized and critical statements concerning them are offered. Although certain questions still remain unanswered, the evidence that near-UV radiation does stimulate cataract formation is very strong. Avoidance of excessive exposure to near-ultraviolet light and the use of protective lenses that filter it out are suggested to prevent the enhancement of human cataract formation by near-UV light.     

Environmental factors in the epidemiology and aetiology of malignant tumours of the eye

This review examines the scientific evidence for and against the role of environmental factors such as acute and accumulative ultraviolet radiation and visible light exposure as causative factors in the development of a spectrum of eye diseases. Displasia and neoplasia are more common in sunny areas and may be due to ultraviolet B radiation. Pale skin, pale iris and a history of squamous cell carcinoma or solar keratoses indicate at-risk patients. Ocular cancer may have an annual age-adjusted incidence between 0.6 per 100,000 and 0.9 per 100,000 for the male population and between 0.5 per 100,000 and 0.8 per 100,000 for the female population.     

Oxidative DNA damage in patients with cataract

Acta Ophthalmol. 2010: 88: 891–895

Abstract.

Purpose: This study examines the levels of oxidative damage in patients with cataract. Methods: Blood samples were collected from 60 patients with cataract and 60 age‐ and gender‐matched healthy individuals to measure 8‐hydroxy 2‐deoxyguanosine (8‐OHdG) and malondialdehyde (MDA) levels. Results: A significant difference was observed in leukocyte 8‐OHdG levels in patients with cataract in comparison with healthy persons (p < 0.001). Similarly, a significant difference was observed in plasma MDA levels in patients with cataract in comparison with healthy persons (p < 0.001). In addition, a significant correlation was found between levels of 8‐OHdG in leukocyte DNA and plasma MDA (r = 0.859, p < 0.001). Conclusion: This study measured the oxidative DNA damage by measuring the 8‐OHdG in the leukocyte DNA in patients with cataract. In addition, the level of MDA – a marker for lipid peroxidation – was measured to determine lipid peroxidation.     

紫外线杀菌灯对小白鼠视网膜的损伤

观察了紫外线杀菌灯照射引起的小白鼠视网膜损伤。在电镜下,发现视网膜色素上皮内含盘膜的吞噬体明显增多;光感受器外段的盘膜有灶状崩溃;内段部分线粒体肿胀;内网织层中空泡形成。     

不同浓度玻璃酸钠对新西兰兔干眼眼表变化的影响

目的：对比观察不同浓度的玻璃酸钠对干眼眼表变化的影响。

方法：制备新西兰兔干眼动物模型,使用1g/L玻璃酸钠和3g/L玻璃酸钠滴滴液治疗,分别作为低浓度治疗组(B组)和高浓度治疗组(C组),生理盐水治疗作为对照组(A组)。分别观察角膜荧光染色、泪液分泌试验、结膜杯状细胞及黏蛋白表达和组织学变化。

结果：治疗后D7和D14时,B组及C组角膜荧光染色评分低于A组(P<0.05),泪液分泌、杯状细胞密度及黏蛋白含量高于A组(P<0.05)。C组角膜泪液分泌和杯状细胞密度高于B组(P<0.05)。与B组和C组相比较,A组角膜及结膜上皮细胞层变薄,角膜及结膜基质未见明显异常。

结论：玻璃酸钠能够改善干眼眼表损害,且高浓度治疗效果优于低浓度。     

Sunlight exposure and pathogenesis of uveal melanoma

Uveal melanoma is the most frequent primary malignant intraocular tumor of adults. Among various non-modifiable risk factors, Caucasian race seems to be the most significant with light skin color, blond hair, and blue eyes being specific risk factors. The racial predisposition to uveal melanoma have been explained on the basis of susceptibility of Caucasian race to oncogenic effects of sunlight. Although there is ample evidence in support of this hypothesis in regard to skin melanoma, the evidence in regard to uveal melanoma is insufficient and contradictory. In the following review, we examine physiologic, epidemiological, and genetic data in order to determine the role of sunlight exposure in the pathogenesis of uveal melanoma.     

氢气的细胞保护作用及其在眼病的应用研究

氢气的还原性能及其医学价值近期引发人们重视.氢气可特异性中和羟自由基和过氧亚硝基阴离子,发挥选择性抗氧化作用.氢气的抗炎症特性可能与多种信号通路相关,它可抑制肿瘤坏死因子-α、促分裂原活化蛋白激酶家族和核因子-κB信号通路来减少炎性介质释放以及炎症细胞趋化,发挥抗炎症作用.氧化应激和炎症反应是多数眼病的共有致病机制,其中氧自由基、炎症因子是介导细胞损伤的重要介质.氢气浓度为0.6 mM的富氢盐水持续点眼或腹腔注射治疗可有效抑制实验动物眼部组织氧化水平,改善缺血再灌注损伤、兴奋性毒性以及糖尿病所致的视网膜退行性改变,抑制碱烧伤导致的角膜新生血管化.氢气治疗作用及其分子机制的深入研究有望为眼病治疗带来新的希望.     

Pre-treatment of adult rats with high doses of erythropoietin induces caspase-9 but prevents light-induced retinal injury

Erythropoietin (Epo) had been shown to have a neuroprotective effect independent from its erythropoietic properties. In this study, we tested whether Epo could protect the retina from damage induced by a long period of moderate light insult and how it protected. First, rats were injected intraperitoneally (i.p.) by human recombinant Epo at 5000 or 30,000U/kg to assess Epo concentration in plasma and retina. Second, rats were untreated or injected i.p. with Epo at 30,000U/kg, 1 or 4h before being placed in constant light (24h; 2200lux). Electroretinograms (ERG) were recorded before treatment, 1day and 15days (D15) after light exposure. After the last ERG, eyes were taken for histology. In parallel, we tested Epo protection against oxidative stressors on isolated retinas and its effect on caspase-9 activity. Epo injected at 30,000U/kg body weight, 4h before exposure to the damaging light, protected retinal function and structure against light damage and induced an increase in caspase-9 activity and expression. Epo had no direct or indirect protective effect against free radicals-induced death on isolated retinas. Epo protected the retina from a long period of moderate light exposure through a mechanism independent from a free radical scavenging property or an antioxidant facilitating activity. The activation of caspase-9, 4h after Epo injection, corresponding to the start of light exposure, suggests that caspase-9 plays a role in neuroprotection.     

Histoplasma capsulatum in the eye

The ocular pathologic findings in an immunosuppressed patient who died of disseminated histoplasmosis are described. Histoplasma capsulatum was found in large numbers within the endothelial cells of the choroid, in one area each of the ciliary body and trabecular meshwork. There was a minimal inflammatory response. No granulomas were noted. Previously reported cases of ocular histoplasmosis in immunosuppressed patients are similar in that, with one exception, granulomatous inflammation was not demonstrated. Thirteen eyes in which histoplasma organisms have been found in the eye are reviewed.     

Lacidipine, thiamine pyrophosphate and their combination on the ocular ischemic syndrome induced by bilateral common carotid artery ligation

AIM: To investigate the effect of lacidipine, thiamine pyrophosphate (TPP) and the combination of lacidipine and TPP against oxidative and inflammatory eye damage induced by bilateral common carotid artery ligation in rats. METHODS: Male albino Wistar rats were categorized as those who underwent sham surgery (SG), right and left common carotid cross-clamping and unclamping procedure (CCU), lacidipine+CCU (LCCU), TPP+CCU (TCCU), and combination of lacidipine and TPP (LTC)+CCU (LTCCU). One hour before anesthesia, the LCCU (n=6) received lacidipine (4 mg/kg, orally) and the TCCU (n=6) received TPP (20 mg/kg, intraperitoneally). The SG (n=6) and CCU (n=6) received the same volume of distilled water from the same route. After anesthesia (60 mg/kg ketamine, intraperitoneally), the necks of the rats were opened in the midline. Ischemia was created for 10min by placing clips on the right and left common carotid arteries. Rats in the SG only underwent subcutaneous incision. After 10min, the clips were removed and reperfusion was achieved for six days. Then, the animals were euthanized (120 mg/kg ketamine, intraperitoneally) and the levels of oxidant, antioxidant and proinflammatory cytokines in the eye tissues were determined. The retinal tissue of the eye was also examined histopathologically. RESULTS: Lacidipine, TPP, and LTC significantly prevent the increase in malondialdehyde, tumor necrosis factor-alpha, interleukin-1β (IL-1β), and IL-6 levels, decrease in total glutathione levels, superoxide dismutase and catalase activities and histopathological retinal damage in eye tissue induced by bilateral common carotid artery ligation in rats. The impact of these drugs on protection is determined to be LTC>lacidipine>TPP. CONCLUSION: As a result of the study, it is concluded that LTC may be more effective than lacidipine and TPP alone in treating ocular ischemic syndrome.     

Increased metallothionein in light damaged mouse retinas

Oxidative stress plays a role in human age-related macular degeneration and in the light damage model of retinal degeneration. Metallothionein (MT), an antioxidant, has been reported to protect retinal pigment epithelial cells against apoptosis and oxidative stress. The purpose of this study was to evaluate changes in MT expression level and retinal localization following light damage. To accomplish this, Balb/c mice were exposed to cool white fluorescent light (10,000 lx) for 7 hr. In three independent experiments, at several intervals after the light injury, retinal MTs were studied at the protein level by immunohistochemistry (IHC) and Western analysis, and at the mRNA level by quantitative PCR with isoform-specific primers. Western analysis and IHC indicated an increase in metallothionein protein following light damage. MT localized to the retinal pigment epithelium and several layers of neural retina. Quantitative PCR identified the expression of MT I-III isoforms, not the MT IV isoform in the mouse retina, and, following light damage, showed increased expression of retinal MT-I and MT-II mRNAs by 8- and 22-fold, respectively. Increased expression of the antioxidant MT in the light damaged mouse retina suggests that upregulation of MT is an important acute retinal response to photo-oxidative stress.     

长期口服抗精神病药物氯氮平对眼表的影响

目的:研究长期使用氯氮平对泪膜稳定性和眼表组织结构的影响。方法:病例对照研究。选取2021-03/12期间接受氯氮平治疗3.45±0.72a的诊断为精神分裂症患者45例(组1)。选取45例健康受试者作为对照组(组2),他们的人口统计学特征与第1组相似。使用OSDI问卷调查患者的干眼症状,SchirmerⅠ试验检测泪液分泌量,眼表染色评分评估眼表损伤情况,并采用LipiView眼表面干涉仪、眼表综合分析仪、角膜共聚焦显微镜和裂隙灯照相系统对所有患者进行全面的眼科检查。结果:裂隙灯照相显示：组1角膜基质可见弥漫性灰白色点状混浊,伴晶状体前囊中央褐色星状混浊。两组OSDI评分分别为38.00(31.50,48.50)、15.00(9.00,19.50)分。Schirmer试验：组1为5.27±2.18mm/5min,组2为15.62±3.05mm/5min。角膜荧光素染色评分：组1为4.00(2.50,5.00)分,组2为1.00(0.00,1.50)分。结膜丽丝胺绿染色评分组1、组2分别为9.00(6.50,10.00)、3.00(2.00,3.50)分。LipiView检测泪膜脂质层厚度...     

硫化氢对眼科疾病潜在治疗作用的研究进展

硫化氢（Ｈ２Ｓ）作为一个新的内源性气体信号分子,参与多种生理与病理效应,如对抗缺血性损伤,减轻氧化应激损伤,抑制细胞凋亡和减轻炎症反应等。目前已从多方面证实了Ｈ２Ｓ的治疗潜能,无论是内源性Ｈ２Ｓ生成还是外源性供给Ｈ２Ｓ,都参与了一系列细胞保护作用。本文综述了Ｈ２Ｓ在一些眼科疾病的病理生理过程中的保护机制。     

Ultraviolet light exposure and its penetrance through the eye in a porcine model

AIM: To determine the amount of ultraviolet (UV) light irradiance that various layers of the eye receive as sunlight passes through the eye, and to investigate the protective benefits of UV light-blocking contact lenses. METHODS: Twenty-four porcine eyes were prepared in one of three ways: isolated cornea, cornea and lens together, or whole eye preparation. UV light irradiance was measured with a UV-A/B light meter before and after the eye preparations were placed over the meter to measure UV light penetration in each eye structure. In the whole eye preparation, a hole was placed in the fovea to measure light as it passed through the vitreous. Subsequently, UV-protective contact lenses were placed over the structures, and UV light penetrance was measured. Measurements of UV light exposure were taken outdoors at various locations and times. RESULTS: Cornea absorbed 63.56% of UV light that reached the eye. Cornea and lens absorbed 99.34% of UV light. Whole eye absorbed 99.77% of UV light. When UV-protective contact lenses were placed, absorption was 98.90%, 99.55%, and 99.87%, respectively. UV light exposure was dependent on directionality and time of day, and was greatest in areas of high albedo that reflect significant amounts of light, such as a beach. CONCLUSION: Cornea absorbs the majority of UV light that reaches the eye in this model. UV-protective contact lenses reduce UV exposure to the eye. Locations with high albedo expose the eye to higher levels of UV light.     

炎症和氧化应激在干眼发病中的作用及干眼的抗炎治疗

干眼在全球的患病率日益增高,其发病机制尚不明确。研究表明炎症和氧化应激是其主要的致病机制。体内和体外的多种刺激因素都会激活氧化应激反应,活性氧水平与抗氧化酶作用的失衡会激活炎症反应,造成眼表组织损伤,最终导致干眼。本文综述炎症和氧化应激在干眼发病中的重要作用及抗炎治疗。     

Oxidative stress-induced mitochondrial DNA damage in human retinal pigment epithelial cells: a possible mechanism for RPE aging and age-related macular degeneration

Oxidative stress is believed to contribute to the pathogenesis of many diseases, including age-related macular degeneration (AMD). Although the vision loss of AMD results from photoreceptor damage in the central retina, the initial pathogenesis involves degeneration of RPE cells. Evidence from a variety of studies suggests that RPE cells are susceptible to oxidative damage. Mitochondrial DNA (mtDNA) is particularly prone to oxidative damage compared to nuclear DNA (nDNA). Using the quantitative PCR assay, a powerful tool to measure oxidative DNA damage and repair, we have shown that human RPE cells treated with H(2)O(2) or rod outer segments resulted in preferential damage to mtDNA, but not nDNA; and damaged mtDNA is not efficiently repaired, leading to compromised mitochondrial redox function as indicated by the MTT assay. Thus, the susceptibility of mtDNA to oxidative damage in human RPE cells, together with the age-related decrease of cellular anti-oxidant system, provides the rationale for a mitochondria-based model of AMD.