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过氧化物酶6对紫外线致大鼠角膜损伤的治疗作用及机制

吕佳惠, 姜敏敏, 石慧, 李建远, 杜振宁

吕佳惠, 姜敏敏, 石慧, 李建远, 杜振宁. 过氧化物酶6对紫外线致大鼠角膜损伤的治疗作用及机制[J]. 中国药科大学学报, 2016, 47(1): 84-89. DOI: 10.11665/j.issn.1000-5048.20160112
引用本文: 吕佳惠, 姜敏敏, 石慧, 李建远, 杜振宁. 过氧化物酶6对紫外线致大鼠角膜损伤的治疗作用及机制[J]. 中国药科大学学报, 2016, 47(1): 84-89. DOI: 10.11665/j.issn.1000-5048.20160112
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LYU Jiahui, JIANG Minmin, SHI Hui, LI Jianyuan, DU Zhenning. Effects and mechanism of peroxiredoxin-6 on ultraviolet-induced corneal injury in rats[J]. Journal of China Pharmaceutical University, 2016, 47(1): 84-89. DOI: 10.11665/j.issn.1000-5048.20160112
Citation: LYU Jiahui, JIANG Minmin, SHI Hui, LI Jianyuan, DU Zhenning. Effects and mechanism of peroxiredoxin-6 on ultraviolet-induced corneal injury in rats[J]. Journal of China Pharmaceutical University, 2016, 47(1): 84-89. DOI: 10.11665/j.issn.1000-5048.20160112
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过氧化物酶6对紫外线致大鼠角膜损伤的治疗作用及机制

  • 1.

    烟台大学药学院

  • 2.

    烟台大学生命科学院

  • 3.

    烟台毓璜顶医院中心实验室

基金项目: 国家自然科学基金资助项目(No.81300738)

Effects and mechanism of peroxiredoxin-6 on ultraviolet-induced corneal injury in rats

摘要

    摘要
  • 摘要: 研究过氧化物酶6(PRDX6)对紫外线照射导致大鼠角膜损伤的治疗作用及其可能的机制。Wister雄性大鼠，紫外线照射法建立大鼠角膜损伤模型，将动物随机分为对照组、PRDX6组和地塞米松(DXM)组，连续给药12 d。通过裂隙灯显微镜检查角膜浑浊度，光学显微镜下观察角膜组织病理学改变，应用硫代巴比妥酸法及化学比色法检测角膜组织丙二醛(MDA)及总抗氧化能力(TAOC)。Western blot检测p38 MAPK信号通路的表达情况，RT-PCR法检测细胞因子基因的表达情况。结果显示，与对照组比较，PRDX6组角膜浑浊度明显降低，病理损伤得到改善，角膜MDA含量减少，TAOC增加，p38 MAPK磷酸化蛋白水平降低，对照组与PRDX6组细胞因子基因的表达有差异(P <；0.05)。结果提示 PRDX6对紫外照射后导致的角膜损伤有一定的治疗作用，这可能与其减轻氧化损伤程度，抑制p38 MAPK磷酸化及调节细胞因子基因表达有关。
    Abstract: To investigate the therapeutic effect of peroxiredoxin-6(PRDX6)on ultraviolet-induced corneal injury in rats and explore the mechanism, a rat model of corneal injury was established by exposing to ultraviolet. Male Wister rats were randomly divided into control group, dexamethasone(DXM)group and PRDX6 group. All the rats were administered four times a day and for 12 days. The corneal opacity was observed with a slit-lamp microscope. Histopathologic changes were observed with light microscope. The content of corneal malonaldehyde(MDA)was determined by thiobarbituric acid test; the total antioxidative capacity(TAOC)was detected by chemical colorimetric test. P38 MAPK signaling pathway was detected with the method of Western blot and gene expression of cytokines was measured by RT-PCR. Compared with the control group, PRDX6 treatment significantly reduced corneal opacity, improved corneal pathology injury, decreased the MDA content and increased the TAOC. In the PRDX6 group, the level of phosphorylated p38 protein was significantly lower than that in the control group. The gene expression of cytokine was different between the control and PRDX6 groups(P < 0. 05). PRDX6 showed therapeutic effect in the rat model of ultraviolet-induced corneal injury, which may be because it could alleviate the oxidative damage, suppress p38 MAPK phosphorylation and regulate the gene expression of cytokine.
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    • 参考文献(14)
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    [2] Chandler HL,Reuter KS,Sinnott LT,et al.Prevention of UV-induced damage to the anterior segment using class I UV-absorbing hydrogel contact lenses[J].Invest Ophthalmol Vis Sci,2010,51(1):172-178.
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  • 刊出日期:  2016-02-24

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