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局部给予过氧化物酶 6 可抑制紫外线辐射诱导的角膜炎症和新生血管形成。

Topical administration of peroxiredoxin-6 on the cornea suppresses inflammation and neovascularization induced by ultraviolet radiation.

机构信息

Institute of Reproductive and Developmental Biology, College of Life Science, Yantai University, Yantai, Shandong Province, People's Republic of China.

出版信息

Invest Ophthalmol Vis Sci. 2012 Dec 7;53(13):8016-28. doi: 10.1167/iovs.12-10064.

Abstract

PURPOSE

To investigate the effect of topical administration of peroxiredoxin-6 (PRDX6) on ultraviolet-induced corneal injury.

METHODS

Corneal transparency and neovascularization were observed with a slit-lamp microscope and hematoxylin and eosin staining. The oxidative damage was determined with a commercial malondialdehyde (MDA) kit. The expressions of PRDX6, polymorphonuclear neutrophil (PMN), vascular endothelial growth factor (VEGF), and pigment epithelium-derived factor (PEDF) were determined by immunohistochemistry and Western blot. The expressions of genes related with antioxidant defense systems and cell apoptosis were detected by RT-PCR.

RESULTS

The irradiated corneas appeared opaque and had high levels of MDA. Peripheral neovascularization and neutrophils appeared in the control and buffer-treated groups (with no treatment or PRDX6 diluent, respectively), whereas they were significantly suppressed in the PRDX6-treated group. The MDA content of the corneas in the PRDX6-treated group was significantly lower than that of the control and buffer-treated groups (P < 0.05). In the PRDX6-treated group the immunoreactivity of VEGF was lower, and that of PEDF was higher, than that in the control and buffer-treated groups. In addition, there were expression correlations between PRDX6 and PMN, VEGF, PEDF. The expressions of genes related with antioxidant defense systems and cell apoptosis were significant different between buffer- and PRDX6-treated groups (P < 0.05).

CONCLUSIONS

The topically administered PRDX6 maintained the homeostasis of corneal cells, reduced inflammation, and suppressed neovascularization and apoptosis under ultraviolet irradiation.

摘要

目的

研究过氧化物酶 6(PRDX6)局部给药对紫外线诱导的角膜损伤的影响。

方法

用裂隙灯显微镜和苏木精-伊红染色观察角膜透明度和新生血管形成。用商业丙二醛(MDA)试剂盒测定氧化损伤。用免疫组织化学和 Western blot 法测定 PRDX6、多形核中性粒细胞(PMN)、血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)的表达。通过 RT-PCR 检测与抗氧化防御系统和细胞凋亡相关的基因表达。

结果

照射后的角膜变得不透明,MDA 水平升高。在对照组和缓冲液处理组(分别为未治疗或 PRDX6 稀释液)中出现了外周血管新生和中性粒细胞,而在 PRDX6 处理组中则明显受到抑制。PRDX6 处理组角膜中的 MDA 含量明显低于对照组和缓冲液处理组(P < 0.05)。在 PRDX6 处理组中,VEGF 的免疫反应性较低,而 PEDF 的免疫反应性较高,明显低于对照组和缓冲液处理组。此外,PRDX6 与 PMN、VEGF、PEDF 之间存在表达相关性。与缓冲液处理组相比,抗氧化防御系统和细胞凋亡相关基因的表达在 PRDX6 处理组中差异显著(P < 0.05)。

结论

局部给予 PRDX6 可维持角膜细胞的内稳态,减少炎症,并抑制紫外线照射下的新生血管形成和凋亡。

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