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巨噬细胞移动抑制因子在小鼠眼部化学伤后眼表疾病发病机制中的作用

The role of macrophage migration inhibitory factor in ocular surface disease pathogenesis after chemical burn in the murine eye.

作者信息

Oh Sei Yeul, Choi Jong-Sun, Kim Eo-Jin, Chuck Roy S, Park Choul Yong

机构信息

Department of Ophthalmology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea.

出版信息

Mol Vis. 2010 Nov 17;16:2402-11.

Abstract

PURPOSE

To evaluate the role of macrophage migration inhibitory factor (MIF) in the wound healing process following severe chemical burns to the ocular surface.

METHODS

Chemical burning of the ocular surface was induced in mice (C57BL/6) via the application of 0.1 M NaOH. Macrophage migration inhibitory factor (MIF), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) mRNA expression in the ocular surface and lacrimal gland was evaluated via real-time reverse transcription PCR on days 2, 7, and 30 after induction of the chemical burn. The expression of MIF protein in the ocular surface and lacrimal gland was evaluated via western blot analysis. Immunohistochemical staining was conducted to detect MIF and vasculoendothelial growth factor in the cornea during the wound healing process. The angiogenic role of MIF was further evaluated using an 8-0 polyglactin suture technique to induce corneal neovascularization.

RESULTS

MIF, TNF-α, and IL-1β mRNA expression were elevated significantly in the ocular surface up to day 30 after chemical burn induction. TNF-α alone was elevated in the lacrimal gland. MIF protein elevation was confirmed via western blot analysis, and the spatial similarity of MIF and VEGF expression in the cornea was noted during the wound healing process. 8-0 polyglactin sutures soaked in MIF induced significantly higher numbers of new vessels on the mouse cornea after 7 days (p=0.003, Mann-Whitney test).

CONCLUSIONS

These findings indicate that MIF performs a crucial role in wound healing on the ocular surface after the induction of chemical burns.

摘要

目的

评估巨噬细胞移动抑制因子(MIF)在严重化学性眼表烧伤后伤口愈合过程中的作用。

方法

通过应用0.1 M氢氧化钠诱导小鼠(C57BL/6)发生眼表化学烧伤。在化学烧伤诱导后的第2天、第7天和第30天,通过实时逆转录聚合酶链反应评估眼表和泪腺中巨噬细胞移动抑制因子(MIF)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的mRNA表达。通过蛋白质印迹分析评估眼表和泪腺中MIF蛋白的表达。在伤口愈合过程中,进行免疫组织化学染色以检测角膜中的MIF和血管内皮生长因子。使用8-0聚乙醇酸缝线技术诱导角膜新生血管形成,进一步评估MIF的血管生成作用。

结果

化学烧伤诱导后直至第30天,眼表中MIF、TNF-α和IL-1β的mRNA表达显著升高。泪腺中仅TNF-α升高。通过蛋白质印迹分析证实了MIF蛋白升高,并且在伤口愈合过程中注意到角膜中MIF和VEGF表达的空间相似性。浸泡在MIF中的8-0聚乙醇酸缝线在7天后诱导小鼠角膜上形成明显更多的新血管(p = 0.003,曼-惠特尼检验)。

结论

这些发现表明,MIF在化学烧伤诱导后眼表伤口愈合中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42a9/2994759/029656113117/mv-v16-2402-f1.jpg

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