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中华眼科医学杂志(电子版) ›› 2021, Vol. 11 ›› Issue (02) : 124 -128. doi: 10.3877/cma.j.issn.2095-2007.2021.02.012

综述

甲状腺相关性眼病氧化应激反应的研究进展
姬璇1, 张朝霞2, 闫春芳3, 孙斌3,()   
  1. 1. 030001 太原,山西医科大学第一临床医学院2018级硕士研究生
    2. 030002 太原,山西省眼科医院中心实验室
    3. 030002 太原,山西省眼科医院眼眶病科
  • 收稿日期:2021-03-26 出版日期:2021-04-28
  • 通信作者: 孙斌
  • 基金资助:
    山西省重点研发计划项目(201903D311009); 山西省中医药管理局传承创新项目(2020ZYYC059)

Advances on the oxidative stress and thyroid associated ophthalmopathy

Xuan Ji1, Zhaoxia Zhang2, Chunfang Yan3, Bin Sun3,()   

  1. 1. Master′s degree 2018, First Clinical Colleage of Shanxi Medical University, Taiyuan 030001, China
    2. Central Laboratory, Shanxi Eye Hospital, Taiyuan 030002, China
    3. Department of Orbital Ophthalmology, Shanxi Eye Hospital, Taiyuan 030002, China
  • Received:2021-03-26 Published:2021-04-28
  • Corresponding author: Bin Sun
引用本文:

姬璇, 张朝霞, 闫春芳, 孙斌. 甲状腺相关性眼病氧化应激反应的研究进展[J]. 中华眼科医学杂志(电子版), 2021, 11(02): 124-128.

Xuan Ji, Zhaoxia Zhang, Chunfang Yan, Bin Sun. Advances on the oxidative stress and thyroid associated ophthalmopathy[J]. Chinese Journal of Ophthalmologic Medicine(Electronic Edition), 2021, 11(02): 124-128.

甲状腺相关性眼病(TAO),是一种与自身免疫性甲状腺病相关的器官特异性自身免疫性疾病。目前,TAO的发病机制尚未完全明确,但已发现氧化应激反应对TAO的发生与发展具有重要影响。炎症和氧化应激恶性循环、酶促抗氧化系统耗竭及多种环境因素作用可诱发TAO的氧化应激反应,促进眼眶成纤维细胞增殖和炎症介质表达。而给予TAO患者硒制剂等抗氧化剂治疗,可以通过抑制氧化应激反应达到改善临床症状的目的。本文中笔者就TAO氧化应激反应的病理改变、发生机制和抗氧化治疗方面的研究现状进行综述。

Thyroid associated ophthalmopathy (TAO) is an organ specific autoimmune disease associated with autoimmune thyroid disease. Currently, the pathogenesis of TAO has not been completely determined, but oxidative stress has been found to have an important impact on the occurrence and development of TAO. The vicious cycle of inflammation and oxidative stress, the depletion of enzymatic antioxidant system and various environmental factors could induce the oxidative stress response of TAO, promote the proliferation of orbital fibroblasts and the expression of inflammatory mediators. The treatment of TAO patients with selenium and other antioxidants could improve the clinical symptoms by inhibiting oxidative stress. In this paper, the pathological changes, pathogenesis and antioxidant treatment of oxidative stress for TAO patients were reviewed.

[1]
Edmunds MR, Boelaert K. Knowledge of Thyroid Eye Disease in Graves′ Disease Patients With and Without Orbitopathy[J]. Thyroid, 2019, 29(4): 557-562.
[2]
Shadel GS, Horvath TL. Mitochondrial ROS signaling in organismal homeostasis[J]. Cell, 2015, 163(3): 560-569.
[3]
Mikhed Y, Görlach A, Knaus UG, et al. Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair[J]. Redox Biol, 2015, 5: 275-289.
[4]
Tsai CC, Wu SB, Cheng CY, et al. Increased oxidative DNA damage, lipid peroxidation, and reactive oxygen species in cultured orbital fibroblasts from patients with Graves' ophthalmopathy: evidence that oxidative stress has a role in this disorder[J]. Eye (Lond), 2010, 24(9): 1520-1525.
[5]
Choi W, Li Y, Ji YS, et al. Oxidative stress markers in tears of patients with Graves' orbitopathy and their correlation with clinical activity score[J]. BMC Ophthalmol, 2018, 18(1): 303.
[6]
Tsai CC, Kao SC, Cheng CY, et al. Oxidative stress change by systemic corticosteroid treatment among patients having active graves ophthalmopathy[J]. Arch Ophthalmol, 2007, 125(12): 1652-1656.
[7]
Tsai CC, Wu SB, Kao SC, et al. The protective effect of antioxidants on orbital fibroblasts from patients with Graves' ophthalmopathy in response to oxidative stress[J]. Mol Vis, 2013, 19: 927-934.
[8]
Lehmann GM, Woeller CF, Pollock SJ, et al. Novel anti-adipogenic activity produced by human fibroblasts[J]. Am J Physiol Cell Physiol, 2010, 299(3): 672-681.
[9]
Dik WA, Virakul S, van Steensel L. Current perspectives on the role of orbital fibroblasts in the pathogenesis of Graves' ophthalmopathy[J]. Exp Eye Res, 2016, 142: 83-91.
[10]
Khong JJ, McNab AA, Ebeling PR, et al. Pathogenesis of thyroid eye disease: review and update on molecular mechanisms[J]. Br J Ophthalmol, 2016, 100(1): 142-150.
[11]
Rotondo DG, Chiarini R, De Gregorio M, et al. Erratum to: Selenium rescues orbital fibroblasts from cell death induced by hydrogen peroxide[J]. Endocrine, 2017, 58(2): 390.
[12]
Rotondo DG, Leo M, Casini G, et al. Antioxidant Actions of Selenium in Orbital Fibroblasts[J]. Thyroid, 2017, 27(2): 271-278.
[13]
Ko J, Kim JY, Lee EJ, et al. Role of binding immunoglobulin protein (BiP) in Graves' orbitopathy pathogenesis[J]. J Mol Endocrinol, 2021, 66(1): 71-81.
[14]
Lee GE, Kim J, Lee JS, et al. Role of Proprotein Convertase Subtilisin/Kexin Type 9 in the Pathogenesis of Graves' Orbitopathy in Orbital Fibroblasts[J]. Front Endocrinol (Lausanne), 2020, 11: 607144.
[15]
Byeon HJ, Kim JY, Ko J, et al. Protein tyrosine phosphatase 1B as a therapeutic target for Graves' orbitopathy in an in vitro model[J]. PLoS One, 2020, 15(8): e0237015.
[16]
Reuter S, Gupta SC, Chaturvedi MM, et al. Oxidative stress, inflammation, and cancer: how are they linked?[J]. Free Radic Biol Med, 2010, 49(11): 1603-1616.
[17]
Londzin-Olesik M, Kos-Kuda B, Nowak A, et al.The effect of thyroid hormone status on selected antioxidant parameters in patients with Graves' disease and active thyroid-associated orbitopathy[J]. Endokrynol Pol, 2020, 71(5): 418-424.
[18]
Kaur A, Pandey S, Kumar S, et al. Oxidative stress profile in graves' ophthalmopathy in Indian patients[J]. Orbit, 2010, 29(2): 97-101.
[19]
Bülow PI, Knudsen N, Carlé A, et al. Serum selenium is low in newly diagnosed Graves' disease[J]. Clin Endocrinol (Oxf), 2013, 79(4): 584-590.
[20]
Khong JJ, Goldstein RF, Sanders KM, et al. Serum selenium status in Graves' disease with and without orbitopathy[J]. Clin Endocrinol (Oxf), 2014, 80(6): 905-910.
[21]
Liu Y, Liu S, Mao J, et al. Serum Trace Elements Profile in Graves' Disease Patients with or without Orbitopathy in Northeast China[J]. Biomed Res Int, 2018: 3029379.
[22]
Wang J, Yang L, Li H, et al. Dietary selenium intake based on the Chinese Food Pagoda[J]. Nutr J, 2018, 17(1): 50.
[23]
Dinh QT, Cui Z, Huang J, et al. Selenium distribution in the Chinese environment and its relationship with human health[J]. Environ Int, 2018, 112: 294-309.
[24]
Carlson BA, Yoo MH, Sano Y, et al. Selenoproteins regulate macrophage invasiveness and extracellular matrix-related gene expression[J]. BMC Immunol, 2009, 10: 57.
[25]
Won HY, Sohn JH, Min HJ, et al. Glutathione peroxidase 1 deficiency attenuates allergen-induced airway inflammation by suppressing Th2 and Th17 cell development[J]. Antioxid Redox Signal, 2010, 13(5): 575-587.
[26]
Diana T, Daiber A, Oelze M, et al. Stimulatory TSH-Receptor Antibodies and Oxidative Stress in Graves Disease[J]. J Clin Endocrinol Metab, 2018, 103(10): 3668-3677.
[27]
Villanueva I, Alva-Sánchez C, Pacheco-Rosado J. The role of thyroid hormones as inductors of oxidative stress and neurodegeneration[J]. Oxid Med Cell Longev, 2013: 218145.
[28]
Gredilla R, López Torres M, Portero-Otín M, et al. Influence of hyper- and hypothyroidism on lipid peroxidation, unsaturation of phospholipids, glutathione system and oxidative damage to nuclear and mitochondrial DNA in mice skeletal muscle[J]. Mol Cell Biochem, 2001, 221(1-2): 41-48.
[29]
Bednarek J, Wysocki H, Sowiński J. Oxidative stress peripheral parameters in Graves' disease: the effect of methimazole treatment in patients with and without infiltrative ophthalmopathy[J]. Clin Biochem, 2005, 38(1): 13-18.
[30]
Marique L, Senou M, Craps J, et al. Oxidative Stress and Upregulation of Antioxidant Proteins, Including Adiponectin, in Extraocular Muscular Cells, Orbital Adipocytes, and Thyrocytes in Graves' Disease Associated with Orbitopathy[J]. Thyroid, 2015, 25(9): 1033-1042.
[31]
Ates I, Yilmaz FM, Altay M, et al. The relationship between oxidative stress and autoimmunity in Hashimoto's thyroiditis[J]. Eur J Endocrinol, 2015, 173(6): 791-799.
[32]
Aydogdu A, Karakas EY, Erkus E, et al. Epicardial fat thickness and oxidative stress parameters in patients with subclinical hypothyroidism[J]. Arch Med Sci, 2017, 13(2): 383-389.
[33]
Citrin D, Cotrim AP, Hyodo F, et al. Radioprotectors and mitigators of radiation-induced normal tissue injury[J]. Oncologist, 2010, 15(4): 360-371.
[34]
Lee SL. Radioactive iodine therapy[J]. Curr Opin Endocrinol Diabetes Obes, 2012, 19(5): 420-428.
[35]
Trayhurn P. Hypoxia and adipose tissue function and dysfunction in obesity[J]. Physiol Rev, 2013, 93(1): 1-21.
[36]
Zhang H, Bosch-Marce M, Shimoda LA, et al. Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia[J]. J Biol Chem, 2008, 283(16): 10892-10903.
[37]
Li HS, Zhou YN, Li L, et al. HIF-1α protects against oxidative stress by directly targeting mitochondria[J]. Redox Biol, 2019, 25: 101109.
[38]
Wang L, Wang B, Chen SR, et al. Effect of Selenium Supplementation on Recurrent Hyperthyroidism Caused by Graves' Disease[J]. Horm Metab Res, 2016, 48(9): 559-564.
[39]
Xu B, Wu D, Ying H, et al. A pilot study on the beneficial effects of additional selenium supplementation to methimazole for treating patients with Graves' disease[J]. Turk J Med Sci, 2019, 49(3): 715-722.
[40]
Zheng H, Wei J, Wang L, et al. Effects of Selenium Supplementation on Graves' Disease[J]. Evid Based Complement Alternat Med, 2018: 3763565.
[41]
Köhrle J. Selenium and the thyroid[J]. Curr Opin Endocrinol Diabetes Obes, 2015, 22(5): 392-401.
[42]
Marcocci C, Kahaly GJ, Krassas GE, et al. Selenium and the course of mild Graves' orbitopathy[J]. N Engl J Med, 2011, 364(20): 1920-1931.
[43]
Negro R, Hegedüs L, Attanasio R, et al. A 2018 European Thyroid Association Survey on the Use of Selenium Supplementation in Graves' Hyperthyroidism and Graves' Orbitopathy[J]. Eur Thyroid J, 2019, 8(1): 7-15.
[44]
Yuan Z, Xu X, Ye H, et al. High levels of plasma selenium are associated with metabolic syndrome and elevated fasting plasma glucose in a Chinese population[J]. J Trace Elem Med Biol, 2015, 32: 189-194.
[45]
Bleys J, Navas-Acien A, Guallar E. Selenium and diabetes: more bad news for supplements[J]. Ann Intern Med, 2007, 147(4): 271-272.
[46]
Lehmann P, Rank P, Hallfeldt KL, et al. Dose-related influence of sodium selenite on apoptosis in human thyroid follicles in vitro induced by iodine, EGF, TGF-beta, and H2O2[J]. Biol Trace Elem Res, 2006, 112(2): 119-130.
[47]
Botta R, Lisi S, Marcocci C, et al. Enalapril reduces proliferation and hyaluronic acid release in orbital fibroblasts[J]. Thyroid, 2013, 23(1): 92-96.
[48]
Lisi S, Botta R, Lemmi M, et al. Quercetin decreases proliferation of orbital fibroblasts and their release of hyaluronic acid[J]. J Endocrinol Invest, 2011, 34(7): 521-527.
[49]
Rotondo Dottore G, Ionni I, Menconi F, et al. Action of three bioavailable antioxidants in orbital fibroblasts from patients with Graves' orbitopathy (GO)[J]. J Endocrinol Invest, 2018, 41(2): 193-201.
[50]
Ko J, Kim JY, Kim JW, et al. Anti-oxidative and anti-adipogenic effects of caffeine in an in vitro model of Graves' orbitopathy[J]. Endocr J, 2020, 67(4): 439-447.
[51]
Li H, Min J, Chen Y, et al. Polydatin attenuates orbital oxidative stress in Graves' orbitopathy through the NRF2 pathway[J]. Chem Biol Interact, 2020, 315: 108894.
[52]
Li H, Gao L, Min J, et al. Neferine suppresses autophagy-induced inflammation, oxidative stress and adipocyte differentiation in Graves' orbitopathy[J]. J Cell Mol Med, 2021, 25(4): 1949-1957.
[53]
Choi YH, Back KO, Kim HJ, et al. Pirfenidone attenuates IL-1β-induced COX-2 and PGE2 production in orbital fibroblasts through suppression of NF-κB activity[J]. Exp Eye Res, 2013, 113: 1-8.
[54]
Lee JS, Chae MK, Kikkawa DO, et al. Glycogen Synthase Kinase-3β Mediates Proinflammatory Cytokine Secretion and Adipogenesis in Orbital Fibroblasts from Patients with Graves' Orbitopathy[J]. Invest Ophthalmol Vis Sci, 2020, 61(8): 51.
[55]
Li H, Yuan Y, Zhang Y, et al. Celastrol inhibits IL-1β-induced inflammation in orbital fibroblasts through the suppression of NF-κB activity[J]. Mol Med Rep, 2016, 14(3): 2799-2806.
[56]
Chen L, Peng Z, Meng Q, et al. Loss of IκB kinase β promotes myofibroblast transformation and senescence through activation of the ROS-TGFβ autocrine loop[J]. Protein Cell, 2016, 7(5): 338-350.
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