龙胆泻肝汤对实验性自身免疫性葡萄膜炎大鼠补体C4、MBL2表达的影响

目的　探讨龙胆泻肝汤（Longdan Xiegan decoction,LXD）对实验性自身免疫性葡萄膜炎(experimental autoimmune uveitis,EAU)大鼠的治疗作用及对血清中C4、MBL2蛋白表达水平的影响。方法　54只Lewis大鼠用随机数字表法分为正常对照组、EAU组和LXD组,其中EAU组、LXD组大鼠制备EAU模型,LXD组造模后使用LXD每天灌胃处理,EAU组给予等量生理盐水灌胃。免疫后12 d使用激光扫描检眼镜（scanning laser ophthalmoscope,SLO）观察三组大鼠眼底炎症,并取三组大鼠同侧眼球进行病理切片,观察视网膜组织病理学变化;分离三组大鼠的脾脏和淋巴结,收集T淋巴细胞,流式细胞仪检测CD4⁺/CD8⁺细胞比例的变化;酶联免疫吸附试验（enzyme-linked immunosorbent assay,ELISA）检测血清中C4、MBL2蛋白的表达水平。结果　SLO检查结果显示,与正常对照组相比,EAU组大鼠屈光间质不清,无法观察眼底视网膜及血管情况;LXD组大鼠眼底血管迂曲扩张,屈光间质混浊,视盘边界模糊不清,但较EAU组大鼠症状轻。组织病理学检查结果显示,与正常对照组相比,EAU组大鼠眼组织结构紊乱,视网膜全层破坏,视网膜内可见大量炎性细胞浸润;LXD组大鼠视网膜仅表现为轻、中度炎性细胞浸润。流式细胞仪检测结果发现,EAU组大鼠脾脏、淋巴结中CD4⁺/CD8⁺比值均高于正常对照组;LXD组大鼠的CD4⁺ T细胞表达水平下降,CD8⁺ T细胞表达水平升高,两者比例趋于平衡。ELISA检测结果发现,与正常对照组相比,EAU组大鼠免疫后12 d、16 d、20 d血清C4蛋白水平均显著升高,与EAU组相比,LXD组免疫后12 d、16 d、20 d血清C4蛋白水平均明显降低,差异均有统计学意义（均为P<0.05）;同时,EAU组各时间点血清MBL2蛋白水平明显降低,而LXD组较EAU组各时间点血清MBL2蛋白水平均显著升高,差异均有统计学意义（均为P<0.01）。结论　LXD可有效缓解EAU大鼠眼内炎症,改善脾脏、淋巴结中CD4⁺/CD8⁺细胞比例失衡,同时降低血清中补体C4蛋白表达水平,上调MBL2蛋白表达水平,促进补体系统恢复平衡,加快葡萄膜炎的炎症消退,从而达到治疗EAU的作用。     

血管生成素对脂多糖诱导的急性葡萄膜炎小鼠的抗炎作用

目的　评价血管生成素(angiogenin,ANG)对小鼠急性葡萄膜炎模型眼部炎症和氧化应激的影响。方法　将BALB/c小鼠随机分为对照组、模型组和ANG组,每组各10只。ANG组小鼠给予ANG滴眼液(100 mg·L^-1·d^-1),对照组和模型组均给予等体积生理盐水。连续给药3 d后,模型组和ANG组在小鼠玻璃体内注射脂多糖(lipopolysaccharide,LPS)建立急性葡萄膜炎模型。125 mg·L^-1 LPS给药24 h后,各组小鼠摘除眼球,收集房水,测量浸润细胞数、总蛋白浓度、一氧化氮(NO)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和氧化应激指数（oxidant stress index,OSI）,并比较各组小鼠炎症反应的程度。结果　与对照组相比,模型组小鼠房水浸润细胞数、总蛋白浓度、NO、TNF-α和IL-6水平、炎症评分、OSI均显著升高(均为P<0.05),而ANG组以上各指标较模型组均显著降低(均为P<0.05)。结论　ANG可通过抑制炎症和氧化应激反应在小鼠急性葡萄膜炎模型中发挥有益作用。     

大鼠眼内组织对内毒素特异敏感的原因

内毒素诱导的葡萄膜炎(endotoxin-induced uveitis,EIU)是革兰氏阴性菌感染相关的人类内源性葡萄膜炎的常用模型。然而在全身注射内毒素诱导的大鼠EIU中,尽管眼内组织表现出明显炎症,但在其它器官组织观察不到明显的病理组织学变化。大鼠眼内组织选择性被内毒素感染的现象提示,其眼内组织对内毒素可能具有某种未知的特殊敏感性。本文就大鼠眼内组织对内毒素特异敏感的可能原因进行综述分析,以期能为临床治疗葡萄膜炎提供新思路。     

蒿甲醚胶丸联合糖皮质激素治疗VKH综合征25例临床观察

目的:探讨蒿甲醚胶丸联合糖皮质激素治疗VKH综合征葡萄膜炎的有效性和安全性。方法:病例回顾性研究,收集25例(50只眼)VKH综合征患者的临床资料,所有患者均接受蒿甲醚胶丸联合糖皮质激素治疗。治疗前及治疗后每1个月随访1次,进行眼部检查和用药不良反应监测。记录矫正视力、炎症情况、眼部并发症及药物不良反应。结果:蒿甲醚胶丸联合糖皮质激素可有效控制葡萄膜炎症,减少眼病并发症,提高矫正视力,延长复发时间;同时全身药物反应较轻。结论:蒿甲醚胶丸联合糖皮质激素治疗VKH综合征安全、有效。     

眼弓蛔虫病诊断与鉴别诊断的临床研究

目的探讨眼弓蛔虫病(OT)诊断与鉴别诊断的方法。 方法收集2016年11月至2021年2月就诊于西安市人民医院(西安市第四医院)眼科，曾在外院误诊的OT患者11例(11只眼)进行研究。其中，男性7例(7只眼)，女性4例(4只眼)；年龄4~47岁，平均年龄(21.4±13.8)岁。采集患者病史，收集临床表现，就诊过程，影像学检查结果，眼内液检测结果。年龄和眼压以 ±s描述。职业、居住地、猫狗接触史、主诉、既往病史、视力、眼部表现、影像学检查结果、眼内液检测结果、诊断及鉴别诊断采用例数(眼数)和百分比进行描述。随访6个月，观察临床诊断是否有修正。 结果11例均为单眼患病。其中，18岁以下者6例(6只眼)，占54.55%(6/11)；18岁以上者5例(5只眼)，占45.45%(5/11)。有玻璃体混浊者11例(11只眼)，占100.00%(11/11)；玻璃体机化分层者7例(7只眼)，占63.64%(7/11)；玻璃体增殖及牵拉性视网膜脱离者4例(4只眼)，占36.36%(4/11)。超声生物显微镜(UBM)检查显示前部玻璃体混浊者4例(4只眼)，占36.36%(4/11)；睫状体后有异常高回声者3例(3只眼)，占27.27%(3/11)，提示周边肉芽肿形成。B型超声检查玻璃体可见异常回声者9例(9只眼)，占81.82%(9/11)。其中，表现为特异性的条索状或带状分层回声者5例(5只眼)，占45.45%(5/11)；表现为点团状回声者4例(4只眼)，占36.36%(4/11)。B型超声显示有牵拉性视网膜脱离者6例(6只眼)，占54.55%(6/11)。荧光素眼底血管造影(FFA)显示视盘着染、荧光素渗漏及视网膜血管显著渗漏者6例(6只眼)，占54.55%(6/11)。其中，表现出视网膜毛细血管"羊齿蕨样"渗漏者3例(3只眼)，占27.27%(3/11)。光学相干断层扫描(OCT)检查结果显示显著黄斑水肿者3例(3只眼)，占27.27%(3/11)。首诊外院误诊为非感染性葡萄膜炎者4例(4只眼)，占36.36%(4/11)；陈旧性视网膜脱离者2例(2只眼)，占18.18%(2/11)；永存原始玻璃体增生症者2例(2只眼)，占18.18%(2/11)；视网膜母细胞瘤者1例(1只眼)，占9.09%(1/11)；黄斑水肿者1例(1只眼)，占9.09%(1/9)；Coat′s病伴新生血管型青光眼者1例(1只眼)，占9.09%(1/11)。眼内液弓蛔虫免疫球蛋白(Ig)G均远高于3U者7例(7只眼)，占63.64%(7/11)。11例(11只眼)OT分型为典型者9例(9只眼)，占81.82%(9/11)。其中，后极部肉芽肿型2例(2只眼)，占18.18%(2/11)；周边肉芽肿型4例(4只眼)，占36.36%(4/11)；眼内炎型3例(3只眼)，占27.27%(3/11)。OT分型为非典型者2例(2只眼)，占18.18%(2/11)。随访6个月以上，临床诊断无修正。 结论OT多为单眼发病，儿童和成人均可患病。OT临床表现复杂多样，可有后极部和(或)周边肉芽肿、眼内炎及玻璃体视网膜增殖等典型表现，B型超声和UBM检查可辅助诊断。也可仅表现为全葡萄膜炎或中间葡萄膜炎，伴黄斑水肿和视网膜毛细血管"羊齿蕨样"渗漏等非典型改变。眼内液弓蛔虫抗体检测对OT诊断具有重要价值。     

Microperimetry findings in patients with birdshot chorioretinopathy

Objective: To assess the role of microperimetry-1 (MPI) as an ancillary tool in patients with birdshot chorioretinopathy (BSCR).Design: Observational cross-sectional study.Participants: Twenty-three eyes of 23 patients.Methods: A review of medical records was conducted of patients with BSCR seen at our institution, from January 2008 to August 2008, on whom MPI had been performed. Of the 23 eyes included in the study, 15 eyes were identified as having HLA-A29 positive BSCR; 8 eyes with no known ocular pathology were used in the analysis as the control group. The clinical status was assessed by biomicroscopy, indirect ophthalmoscopy, and fluorescein angiography.Results: When eyes with active disease were compared with eyes with inactive disease there was a statistically significant difference (p = 0.001) between them in the number of points below 16 dB. The difference was also statistically significant (p = 0.04) when it was adjusted for visual acuity, associated disease, and age. When eyes of patients with inactive disease were compared with control eyes, there was a statistically significant difference (p = 0.01) in the number of points below 16 dB, suggesting that not all patients may recover their full retinal sensitivities. When eyes of patients with active disease were compared with controls there was a statistically significant difference (p = 0.01) between them in the number of points below 16 dB after adjusting for age, visual acuity, and associated disease (macular edema and epiretinal membrane).Conclusions: Microperimetric quantification of macular sensitivity in patients with BSCR may provide an ancillary tool to evaluate activity and may help to assess visual impairment in these patients.     

Orally induced,peptide-specific γ/δ TCR+ cells suppress experimental autoimmune uveitis

We investigated the role of γ/δ TCR⁺ T cells in induction and suppression of the T cell-mediated disease experimental autoimmune uveitis. Disease induction was studied in Lewis rats perinatally depleted of α/β or γ/δ TCR⁺ subpopulations. Depletion of α/δ TCR⁺ cells completely abrogated disease, whereas treatment with anti-γ/δ antibodies had no influence on onset or intensity of uveitis. However, adoptively transferred γ/δ⁺ cells from orally tolerized rats could mediate suppression of uveitis in an antigen-specific fashion. Uveitis induced by a peptide derived from the uveitogenic retinal soluble antigen (S-Ag) was suppressed by γ/δ⁺ cells from rats orally tolerized with the same peptide as well as HLA peptide B27PD. This disease ameliorating effect could also be observed when rats were fed with the HLA peptide before immunization with S-Ag peptide. Transfer of α/β⁺ T cells from the same donors as well as γ/δ⁺ or α/β⁺ cells from animals fed with control peptide had no ameliorating effect.     

Effects of heme oxygenase-1 inducer and inhibitor on experimental autoimmune uveoretinitis

PURPOSE: Experimental autoimmune uveoretinitis (EAU) is an animal model of posterior uveitis and heme oxygenase-1 (HO-1) is a well-known anti-oxidant factor. However, there is no report a protective role of HO-1 on EAU in vivo. To verify that HO-1 is induced in EAU by interphotoreceptor retinoid-binding protein (IRBP), that an HO-1 inducers ameliorates the associated inflammation, and that an HO-1 inhibitor exacerbates this inflammation. METHODS: Forty four Lewis rats were given either 40 mol/kg hemin or 40 mol/kg SnPP (tin protoporphyrin IX) by intraperitoneal injection and twenty two uveitis control rats were injected with 0.5 mL of saline once daily 5-20 days after IRBP immunization inducing EAU. Three normal control rats were used for Western blotting and ELISA assay of HO-1. The clinical uveitis signs of inflammation were scored in the three groups from 0 to 4 on alternate three days. To confirm the clinical results, histological and immunohistochemical stain of HO-1 were performed on the day of peak inflammation and Western blotting and ELISA assay of HO-1 were performed on 6th, 12th and 18th day after IRBP immunization. RESULTS: Hemin, an inducer of HO-1, ameliorated the clinical signs of EAU. In contrast, SnPP-treated rats show that the severity of the clinical sign were exacerbated at the peak period of the disease. These results are roughly compatible with histological, immunoblotting, and immunohistochemical evaluations and an ELISA assay of HO-1. CONCLUSIONS: We suggest that HO-1 plays an important protective role in EAU.