T细胞和b细胞缺乏对急性高眼压小鼠视网膜神经细胞的影响

Y. Huo, Ping Huang, Shaomin Zhang, Chun Zhang
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引用次数: 1

摘要

背景近年来,对青光眼致视神经损伤原因的研究一直是眼科关注的热点。一些研究表明免疫系统与青光眼引起的视神经病变有关。急性缺血再灌注是研究视神经病变的理想模型。目的探讨T淋巴细胞和B淋巴细胞缺乏对急性高眼压小鼠视网膜神经细胞的影响。方法选用6 ~ 8周龄SPF CB-17/Icr.Cg-Prkdc~(scid)Lyst~(bg)/CrlVR小鼠16只,与年龄匹配的SPF野生型(C57BL/6)小鼠16只作对照。10只SCID小鼠和10只C57BL/6小鼠右眼通过前房灌注平衡生理盐水45min使眼压升高至104mmHg,建立缺血再灌注损伤模型,左眼作为模型对照。另外6只SCID小鼠和6只C57BL/6小鼠作为正常对照组。在小鼠脑内注射10g/L (2μL)的FlouroGold,标记缺血再灌注21天后存活的视网膜神经节细胞。缺血21 d后,荧光显微镜下H&E染色测定视网膜内核层厚度。动物的使用遵循视力和眼科研究协会的标准。结果在正常对照小鼠中,SCID小鼠和C57BL/6小鼠的视网膜神经节细胞(RGCs)形态和视网膜结构相似。两组小鼠RGCs数量和视网膜厚度差异无统计学意义(P>0.05)。在实验小鼠中,与C57BL/6小鼠(78%±5%)相比,SCID小鼠存活的RGCs显著增加(91%±5%)(P=0.003)。C57BL/6小鼠模型眼视网膜内核层厚度(22.44±1.70μm)明显薄于C57BL/6小鼠模型眼(31.06±3.75μm) (P=0.004),而SCID小鼠模型眼与模型眼(33.52±2.13μm vs 34.06±3.00μm)在缺血再灌注损伤21 d后差异无统计学意义(P>0.05)。结论T淋巴细胞和B淋巴细胞缺陷小鼠对急性高眼压的耐受性优于野生型C57BL/6小鼠。关键词:急性高眼压;视网膜神经节细胞;免疫缺陷;视网膜缺血再灌注
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Influence of T- and B-cell-deficiency on retinal neurocytes of mice withacute ocular hypertension
Background Recently,the study on the cause of optic nerve damage induced by glaucoma is of concern in ophthalmology.Some research showed that the immune system is associated with glaucoma-induced optic neuropathy.Acute ischemia-reperfusion is an ideal model of studying optic neuropathy.ObjectiveThe present study investigates the effect of T and B lymphocyte deficiency on the retinal neurocytes of mice with acute intraocular hypertension.Methods Sixteen SPF CB-17/Icr.Cg-Prkdc~(scid)Lyst~(bg)/CrlVR mice 6-8 week-old (severe combined immunodeficiency mouse,SCID) were used in this study and 16 age-matched SPF wild type (C57BL/6) mice served as controls.The ischemia-reperfusion injury models were induced in the right eyes of 10 SCID mice and 10 C57BL/6 mice through intra-anterior chamber infusion of balanced saline solution for 45minutes to increase the intraocular pressure to 104mmHg,and the left eyes served as model controls.The other 6 SCID mice and 6 C57BL/6 mice served as normal control group.10g/L (2μL) of FlouroGold was injected into the brains of the mice for the labeling of surviving retinal ganglion cells 21 days after ischemia-reperfusion.The thickness of retinal inner nuclear layer was measured by H&E staining under the fluorescent microscope 21 days after ischemic insult.The use of the animals followed the Standard of Association for Research in Vision and Ophthalmology.Results In normal control mice,the morphology of retinal ganglion cells (RGCs) and retinal structure were similar between SCID mice and C57BL/6 mice.The differences in the numbers of RGCs and retinal thickness were insignificant between the two types of mice(P>0.05).In the experimental mice,the surviving RGCs were strikingly increased in SCID mice (91%±5%) compared with C57BL/6 mice(78%±5%)(P=0.003).The thickness of the retinal inner nuclear layer was obviously thinner in the model eyes (22.44±1.70μm) compared to model control eyes (31.06±3.75μm) in C57BL/6 mice(P=0.004),but no statistically significant difference was found between the model eyes and model control eyes in SCID mice (33.52±2.13μm vs 34.06±3.00μm) 21 days after ischemia-reperfusion injury(P>0.05).Conclusion T and B lymphocytes deficient mice show a better tolerance to acute intraocular hypertension than the wild type C57BL/6 mice. Key words: acute ocular hypertension; retina ganglion cells; immunodeficient; retinal ischemia-reperfusion
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