普拉洛芬在干眼中对Th1细胞趋化因子受体CXCR3和CCR5表达的影响

doi:DOI:10.3760/cma.j.issn.1674-845X.2017.06.009

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摘要

目的：观察普拉洛芬对Th1 细胞CXC趋化因子受体3（CXCR3）和CC趋化因子受体5（CCR5）表达的影响，并探讨其抑制干眼炎症免疫反应的机制。方法：随机对照试验。纳入干眼患者170例（170眼），均选取右眼为观察眼。采用随机数字表法分为试验组和对照组，各85 例（85 眼）。试验组予普拉洛芬联合玻璃酸钠点眼，均每日4次，每次1滴；对照组仅玻璃酸钠点眼，每日4次，每次1滴。于治疗前和治疗后30 d时进行随访，检测并比较2 组泪液分泌量（SIt）、泪膜破裂时间（BUT）、角膜荧光素染色（CFS）评分，CXCR3和CCR5 表达率，及两者与BUT和CFS关系。采用Pearson直线相关分析以及t 检验对数据进行分析。结果：治疗后2 组BUT均较治疗前延长（t =-13.27、-13.53，均P ＜0.05），且试验组长于对照组（t =10.11，P ＜0.05）；治疗后2组CFS评分均低于治疗前（t =7.34、5.27，均P ＜0.05），且试验组低于对照组（t =5.15，P ＜0.05）；治疗后试验组CXCR3、CCR5的表达率低于治疗前（t =6.74、9.27，均P ＜0.05），且试验组低于对照组（t =3.29、2.83，均P ＜0.05）；试验组CXCR3、CCR5表达率与BUT呈负相关（r =-0.22、-0.22，均P ＜0.05），与CFS评分呈正相关（r =0.28、0.23，均P ＜0.05）。结论：普拉洛芬可通过下调眼表Th1细胞CXCR3和CCR5的表达来发挥对干眼的治疗作用。

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关键词 ：干眼, 普拉洛芬, CXC型趋化因子受体3, CC型趋化因子受体5, 趋化因子

Abstract：

Objective: To investigate the effect of pranoprofen on the expression of CXC chemokine receptor 3(CXCR3) and CC chemokine receptor 5 (CCR5) of Th1 cells in dry eye patients, and to explore thecorrelation of changes in receptor expression with clinical changes of dry eye signs. Methods: This study
included 170 patients with dry eye in a randomized, controlled clinical trial. The right eyes of the patients (n=85) administered 0.1% pranoprofen and 0.1% sodium hyaluronate drops (4 times/day). The right eyes of the control dry eye patients (n=85) received 0.1% sodium hyaluronate drops alone (4 times/day). The two groups were followed up before administration and 30 days later. The primary clinical indexes thatwere evaluated included Schirmer I test (SIt), tear film break-up time (BUT), and corneal fluorescein staining (CFS). Differences in the expression of CXCR3 and CCR5 were compared between the two groups. Changes in the expression levels of CXCR3 and CCR5 were correlated with changes in SIt, BUT, and FIS. The data were analyzed by t test and pearson correlation. Results: The tear BUT was significantly longer in both groups after treatment compared to the pretreatment values (t=-13.27, -13.53, both P <0.05). Additionally, the tear BUT was significantly longer in the pranoprofen-treated test group compared to the control group (t=10.11, P <0.05). The CFS scores in both groups were lower than before treatment (t=7.34, 5.27, both P <0.05), and it was significantly lower in the test group compared with the control group (t=5.15,P<0.05). Expression levels of both CXCR3 and CCR5 were significantly reduced in the test group than pretreatment (t=6.74, 9.27, both P <0.05), and it was significantly lower in the test group, compared with the pretreatment values (t=3.29, 2.83, both P <0.05). The expression levels of both CXCR3 and CCR5 were negatively correlated with BUT (r=-0.22, -0.22, both P <0.05) and positively correlated with CFS (r=0.28,0.23, both P <0.05).Conclusion: Pranoprofen inhibits the inflammatory immune response in dry eye bydown-regulating the expression of the chemokine receptors CXCR3 and CCR5 on Th1 cells.

Key words： dry eye pranoprofen CXC chemokine receptor 3 CC chemokine receptor 5 chemokine

收稿日期: 2017-03-06

基金资助:

乌鲁木齐市科学技术计划项目（Y131310003）

通讯作者: 张宏，Email：nature2735@163.com

引用本文:

蔡丽萍,刘雅琴,孟然,张宏. 普拉洛芬在干眼中对Th1细胞趋化因子受体CXCR3和CCR5表达的影响[J]. 中华眼视光学与视觉科学杂志, 2017, 19(6): 364-368. Liping Cai1,2, Yaqin Liu1, Ran Meng1, Hong Zhang1. Effect of Pranoprofen on the Expression of Chemokine Receptors CXCR3 and CCR5 of Th1 Cells in Dry Eye Patients. Chinese Journal of Optometry Ophthalmology and Visual science, 2017, 19(6): 364-368. DOI: DOI:10.3760/cma.j.issn.1674-845X.2017.06.009

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[1]	Barabino S, Chen Y, Chauhan S, et al. Ocular surface immunity: homeostatic mechanisms and their disruption in dry eye disease. Prog Retin Eye Res, 2012, 31(3): 271-285. DOI: 10.1016/j.preteyeres. 2012.02.003.
[2]	SternME,SchaumburgCS,PflugfelderSC.Dryeyeasamucosal autoimmune disease. Int Rev Immunol, 2013, 32(1): 19-41. DOI:10.3109/08830185.2012.748052.
[3]	张宏, 孙勇, 安晓, 等. 干眼与CC趋化因子受体5和CXC趋化因子受体3及其配体介导的炎性反应的关系. 中华实验眼科杂志, 2015, 33(7): 633-637. DOI: 10.3760/cma.j.issn. 2095-0160.2015. 07.013.
[4]	刘雅琴, 李晶, 具尔提 ·阿不都卡地尔, 等. 普拉洛芬联合玻璃酸钠治疗干眼的临床疗效观察. 新疆医科大学学报, 2016, 39(4): 456-459. DOI: 10.3969/j.issn.1009-5551.2016.04.018.
[5]	陈景尧, 谢立信, 刘祖国, 等. 普拉洛芬治疗轻中度干眼的多中心随机对照临床试验. 中华实验眼科杂志, 2015, 33(9): 834-839. DOI: 10.3760/cma.j.issn.2095-0160.2015.09.018.
[6]	李东辉, 龙琴, 卞爱玲, 等. 普拉洛芬滴眼液治疗中重度干眼的随机对照研究. 中华实验眼科杂志, 2012, 30(5): 445-449. DOI: 10.3760/cma.j.issn.2095-0160.2012.05.014.
[7]	Fiorelli VM, Bhat P, Foster CS. Nonsteroidal anti-inflammatory therapyandrecurrentacuteanterioruveitis.OculImmunolInflamm 2010, 18(2): 116-120. DOI: 10.3109/09273941003587558.
[8]	PflugfelderSC,CorralesRM,dePaivaCS.Thelpercytokinesindryeye disease. Exp Eye Res, 2013, 117: 118-125. DOI: 10.1016/j.exer.2013.08.013.
[9]	朱俊雕, 陈雪燕, 陈雪艺. 新疆维吾尔族干眼症与趋化因子受体?鄄5的相关性研究. 国际眼科杂志, 2012, 12(1): 43 -45. DOI: 10.3969/ j.issn.1672-5123.2012.01.13.
[10]	Yoon KC, Park CS, You IC, et al. Expression of CXCL9, -10, -11, and CXCR3 in the tear film and ocular surface of patients with dry eye syndrome. Invest Ophthalmol Vis Sci, 2010, 51(2): 643-650. DOI: 10.1167/iovs.09-3425.
[11]	Coursey TG, Gandhi NB, Volpe EA, et al. Chemokine receptors CCR6 and CXCR3 are necessary for CD4(+) T cell mediated ocular surface disease in experimental dry eye disease. PLoS One, 2013, 8(11): e78508. DOI: 10.1371/journal.pone.0078508.
[12]	Karin N, Wildbaum G, Thelen M. Biased signaling pathways via CXCR3 control the development and function of CD4+T cell subsets. J Leukoc Biol, 2016, 99(6): 857-862. DOI: 10.1189/ jlb.2MR0915-441R.
[13]	Coursey TG, Bohat R, Barbosa FL, et al. Desiccating stress- induced chemokine expression in the epithelium is dependent on upregulation of NKG2D/RAE-1 and release ofIFN-γin experimentaldry eye. J Immunol, 2014, 193(10): 5264-5272. DOI: 10.4049/jimmunol.1400016.
[14]	Zohar Y, Wildbaum G, Novak R, et al. CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis. J Clin Invest, 2014, 124(5): 2009-2022. DOI: 10.1172/JCI71951.