[1]尹贻雪,焦路光,王嘉睿,等.红外激光致角膜损伤的修复机制研究[J].眼科新进展,2024,44(5):350-354.[doi:10.13389/j.cnki.rao.2024.0068]
 YIN Yixue,JIAO Luguang,WANG Jiarui,et al.Corneal wound healing mechanism after infrared laser irradiation[J].Recent Advances in Ophthalmology,2024,44(5):350-354.[doi:10.13389/j.cnki.rao.2024.0068]
点击复制

红外激光致角膜损伤的修复机制研究/HTML
分享到:

《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
44卷
期数:
2024年5期
页码:
350-354
栏目:
实验研究
出版日期:
2024-04-30

文章信息/Info

Title:
Corneal wound healing mechanism after infrared laser irradiation
作者:
尹贻雪焦路光王嘉睿周聪伶杨在富
250014 山东省济南市,山东中医药大学附属眼科医院(尹贻雪);100850 北京市,军事科学院军事医学研究院辐射医学研究所(尹贻雪,焦路光,王嘉睿,周聪伶,杨在富);230032 安徽省合肥市,安徽医科大学基础医学院(尹贻雪,杨在富)
Author(s):
YIN Yixue123JIAO Luguang2WANG Jiarui2ZHOU Congling2YANG Zaifu23
1.Affiliated Eye Hospital of Shandong University of Traditional Chinese Medicine,Jinan 250014,Shandong Province,China
2.Institute of Radiation Medicine,Academy of Military Medical Sciences,Academy of Military Sciences,Beijing 100850,China
3.School of Basic Medical Sciences,Anhui Medical University,Hefei 230032,Anhui Province,China
关键词:
红外激光角膜损伤损伤修复免疫组织化学染色
Keywords:
infrared laser corneal injury wound healing immunohistochemical staining
分类号:
R779.1
DOI:
10.13389/j.cnki.rao.2024.0068
文献标志码:
A
摘要:
目的 探讨3.74 μm红外激光致角膜损伤的修复机制。
方法 取27只6~8周龄C57BL/6J小鼠作为研究对象,将小鼠随机分为正常组(3只)和实验组(24只)。正常组不做任何处理,实验组小鼠用3.74 μm 红外激光照射双眼,光斑直径2 mm,曝光时间0.8 s,辐照量23.2 J·cm-2。激光照射损伤后3 h、6 h、12 h、1 d、3 d、7 d、14 d、21 d各取3只实验组小鼠,连同正常组小鼠角膜组织进行病理切片,采用免疫组织化学染色检测中性粒细胞弹性蛋白酶、CD68、CD163以及血栓调节蛋白阳性细胞情况,鉴定新生血管发生情况。
结果 正常组小鼠角膜基质中均未见中性粒细胞弹性蛋白酶、CD68、CD163以及血栓调节蛋白阳性细胞。实验组小鼠中性粒细胞弹性蛋白酶阳性细胞在激光照射后3 h出现于角膜组织损伤边缘,12 h迁移至损伤区,1 d时数量最多,之后逐渐减少,21 d仍有少量阳性细胞;CD68阳性细胞在激光照射后12 h出现于角膜组织损伤边缘,1 d时出现在损伤区,21 d时仍有少量阳性细胞;CD163阳性细胞在激光照射后7 d出现于角膜组织损伤边缘,14 d时出现在损伤区,21 d仍有少量阳性细胞;血栓调节蛋白阳性细胞在激光照射后14~21 d出现于角膜基质损伤区。
结论 3.74 μm红外激光可致角膜全层损伤,大量炎症细胞自损伤边界或角膜缘向损伤区迁移并参与修复过程。早期以中性粒细胞和M1型巨噬细胞浸润为主,后期以M2型巨噬细胞参与为主,并伴有新生血管生成。
Abstract:
Objective To explore the corneal wound healing mechanism after 3.74 μm infrared laser irradiation.
Methods Twenty-seven C57BL/6J mice (six to eight weeks old) were randomly divided into a normal group (3 mice) and an experimental group (24 mice). Mice in the normal group were not subjected to any treatment. The corneas of mice in the experimental group were damaged by infrared laser at a wavelength of 3.74 μm. The spot diameter was 2 mm, the exposure duration 0.8 s, and the radiant exposure 23.2 J·cm-2. Pathological sectioning of corneas was performed at 3 h, 6 h, 12 h, 1 d, 3 d, 7 d, 14 d, and 21 d after laser irradiation in the experimental group, with 3 mice at each time point. It was the same for mice in the normal group. Immunohistochemical staining was conducted to examine neutrophil elastase, CD68, CD163 and thrombomodulin-positive cells and identify neovascularization.
Results Neutrophil elastase, CD68, CD163, and thrombomodulin-positive cells were not detected in the corneal stroma of mice in the normal group. Neutrophil elastase-positive cells were detected in the damaged corneal periphery of mice in the experimental group at 3 h, migrated to the damaged area at 12 h, peaked at 1 d, and then decreased gradually with time, but still existed slightly at 21 d after laser irradiation. CD68-positive cells were detected in the damaged corneal periphery of mice in the experimental group at 12 h and in the damaged area at 1 d through 21 d after laser irradiation. CD163-positive cells were found in the damaged corneal periphery of mice in the experimental group at 7 d and in the damaged area at 14 d and 21 d after laser irradiation. Thrombomodulin-positive cells were found in the damaged area of the corneal stroma at 14 d and 21 d after laser irradiation.
Conclusion During the wound healing process after 3.74 μm infrared laser-induced full-thickness corneal injury in mice, a large number of inflammatory cells migrate from the damaged corneal periphery or limbus to the damaged area. Neutrophils and M1 macrophages infiltrate in the early stage, while M2 macrophages are involved in the later stage, accompanied by neovascularization.

参考文献/References:

[1] VAINIO M,SILTANEN M,PELTOLA J,HALONEN L.Grating-cavity continuous-wave optical parametric oscillators for high-resolution mid-infrared spectroscopy[J].Appl Opt,2011,50(4):A1-A10.
[2] WILLER U,SARAJI M,KHORSANDI A,GEISER P,SCHADE W.Near- and mid-infrared laser monitoring of industrial processes,environment and security applications[J].Opt Lasers Eng,2006,44(7):699-710.
[3] TUTTLE R.Large aircraft infrared countermeasures system[J].Aerosp Daily Def Rep,2004,210(7):6-7.
[4] GROSS P,KLEIN M E,WALDE T,BOLLER K J,AUERBACH M,WESSELS P,et al.Fiber-laser-pumped continuous-wave singly resonant optical parametric oscillator[J].Opt Lett,2002,27(6):418-420.
[5] HENDERSON A,STAFFORD R.Low threshold,singly-resonant CW OPO pumped by an all-fiber pump source[J].Opt Express,2006,14(2):767-772.
[6] VAINIO M,PELTOLA J,PERSIJN S,HARREN F J,HALONEN L.Singly resonant cw OPO with simple wavelength tuning[J].Opt Express,2008,16(15):11141-11146.
[7] RAMAIAH-BADARLA V,KUMAR S C,EBRAHIM-ZADEH M.Fiber-laser-pumped,dual-wavelength,picosecond optical parametric oscillator[J].Opt Lett,2014,39(9):2739-2742.
[8] 晏程,王海兰,江嘉欣,陈青松,严茂胜,陈嘉斌.激光致眼损伤机制研究进展[J].中国职业医学,2015,42(1):85-88,92.
YAN C,WANG H L,JIANG J X,CHEN Q S,YAN M S,CHEN J B.Research progress on ophthalmic injuries caused by laser[J].China Occup Med,2015,42(1):85-88,92.
[9] INTERNATIONAL COMMISSION ON NON-IONIZING RADIATION PROTECTION (ICNIRP).ICNIRP guidelines on limits of exposure to laser radiation of wavelengths between 180 nm and 1,000 μm[J].Health Phys,2013,105(3):271-295.
[10] 杨在富,王嘉睿,陈虹霞,景小敏,杨景庚,张笑明.脉冲1.338 μm 激光角膜损伤效应研究[J].激光生物学报,2012,21(6):497-501.
YANG Z F,WANG J R,CHEN H X,JING X M,YANG J G,ZHANG X M.Corneal Injury Induced by Pulsed 1.338 μm Laser Radiation[J].Acta Laser Biol Sin,2012,21(6):497-501.
[11] WANG J,JIAO L,CHEN H,YANG Z,HU X.Corneal thermal damage threshold dependence on the exposure duration for near-infrared laser radiation at 1319 nm[J].J Biomed Opt,2016,21(1):15011.
[12] JIAO L,WANG J,JING X,CHEN H,YANG Z.Ocular damage effects from 1338-nm pulsed laser radiation in a rabbit eye model[J].Biomed Opt Express,2017,8(5):2745-2755.
[13] CHEN H,YANG Z,WANG J,CHEN P,QIAN H.A comparative study on ocular damage induced by 1319nm laser radiation[J].Lasers Surg Med,2011,43(4):306-312.
[14] JIAO L,WANG C,ZHANG K,WANG J,YANG Z.Corneal damage effects induced by infrared optical parametric oscillator radiation at 3743 nm[J].J Innov Opt Health Sci,2021,14(2):215004.
[15] 王超,焦路光,王嘉睿,尹贻雪,杨在富.波长3.74 μm激光致兔角膜损伤及其修复研究[J].军事医学,2022,46(4):273-279.
WANG C,JIAO L G,WANG J R,YIN Y X,YANG Z F.Corneal injury effect and wound healing in rabbits after 3.74 μm laser irradiation[J].Mill Med Sci,2022,46(4):273-279.
[16] 尹贻雪,焦路光,王嘉睿,王超,任子淇,赵乙珑,等.3.74 μm远红外激光致小鼠角膜损伤修复观察[J].激光生物学报,2022,31(3):261-267.
YIN Y X,JIAO L G,WANG J R,WANG C,REN Z Q,ZHAO Y L,et al.Observation of mice corneal wound healing after 3.74 μm laser irradiation[J].Acta Laser Biol Sin,2022,31(3):261-267.
[17] 伍志琴,杨燕宁,邢怡桥,袁静,杨万举.小鼠单纯疱疹病毒性角膜炎中基质金属蛋白酶-2、8、9阳性细胞计数及意义[J].中华临床医师杂志(电子版),2011,5(2):417-422.
WU Z Q,YANG Y N,XING Y Q,YUAN J,YANG W J.Expression and clinical significance of matrix metalloproteinases-2,8,9 positive cells in murine herpes stromal keratitis[J].Chin J Clinicians(Electron Edition),2011,5(2):417-422.
[18] LI Y,WANG Y,LI C,ZHAO D,HU Q,ZHOU M,et al.The role of elastase in corneal epithelial barrier dysfunction caused by Pseudomonas aeruginosa exoproteins[J].Invest Ophthalmol Vis Sci,2021,62(9):7.
[19] JUSTET C,EVANS F,TORRIGLIA A,CHIFFLET S.Increase in the expression of leukocyte elastase inhibitor during wound healing in corneal endothelial cells[J].Cell Tissue Res,2015,362(3):557-568.
[20] HUANG W,WEI X,WEI Y,FENG R.Biology of tumor associated macrophages in diffuse large B cell lymphoma[J].DNA Cell Biol,2018,2018:4374.
[21] RUFFELL B,AFFARA N I,COUSSENS L M.Differential macrophage programming in the tumor microenvironment[J].Trends Immunol,2012,33(3):119-126.
[22] 张志斌,朱艳,席俊峰.CD68+、CD163+巨噬细胞对食管癌浸润及预后的影响[J].现代中西医结合杂志,2015,24(6):590-592.
ZHANG Z B,ZHU Y,XI J F.Influence of CD68+ and CD163+ macrophages on the infiltration of esophageal carcinoma and its prognosis[J].Mod J Integr Tradit Chin West Med,2015,24(6):590-592.
[23] ZHANG S X,MA J X.Ocular neovascularization:implication of endogenous angiogenic inhibitors and potential therapy[J].Prog Retin Eye Res,2007,26(1):1-37.
[24] 高世凯,崇晓霞.角膜新生血管形成的分子生物学研究进展[J].医学综述,2013,19(2):207-210.
GAO S K,CHONG X X.Research progress in molecular biology of corneal neovascularization[J].Med Recapitul,2013,19(2):207-210.
[25] GORDON S,MARTINEZ F O.Alternative activation of macrophages:mechanism and functions[J].Immunity,2010,32(5):593-604.
[26] HAN Y,SHEN M,TANG L Y,TAN G,YANG Q C,YE L,et al.Antiangiogenic effects of catalpol on rat corneal neovascularization[J].Mol Med Rep,2018,17(2):2187-2194.
[27] UCHIYAMA M,SHIMIZU A,MASUDA Y,NAGASAKA S,FUKUDA Y,TAKAHASHI H.An ophthalmic solution of a peroxisome proliferator-activated receptor gamma agonist prevents corneal inflammation in a rat alkali burn model[J].Mol Vis,2013,19:2135-2150.
[28] HAN Y,SHAO Y,LIN Z,QU Y L,WANG H,ZHOU Y,et al.Netrin-1 simultaneously suppresses corneal inflammation and neovascularization[J].Invest Ophthalmol Vis Sci,2012,53(3):1285-1295.
[29] CHOI H,PHILLIPS C,OH J Y,STOCK E M,KIM D K,WON J K,et al.Comprehensive modeling of corneal alkali injury in the rat eye[J].Curr Eye Res,2017,42(10):1348-1357.

相似文献/References:

[1]严宏,陈曦,陈颖.白内障术后并发症:现状与对策[J].眼科新进展,2019,39(1):001.[doi:10.13389/j.cnki.rao.2019.0001]
 YAN Hong,CHEN Xi,CHEN Ying.Postoperative complications of cataract:current status and countermeasures[J].Recent Advances in Ophthalmology,2019,39(5):001.[doi:10.13389/j.cnki.rao.2019.0001]

备注/Memo

备注/Memo:
国家自然科学基金项目(编号:61575221)
更新日期/Last Update: 2024-05-05