首页> 外文期刊>Japanese Journal of Ophthalmology >Abnormal deposition of laminin and type IV collagen at corneal epithelial basement membrane during wound healing in diabetic rats.
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Abnormal deposition of laminin and type IV collagen at corneal epithelial basement membrane during wound healing in diabetic rats.

机译:糖尿病大鼠伤口愈合过程中层粘连蛋白和IV型胶原在角膜上皮基底膜上的异常沉积。

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PURPOSE: To understand the pathophysiology of the corneal basement membrane in diabetes, we compared the localization of laminin and type IV collagen in the epithelial basement membrane during corneal epithelial wound healing in diabetic and nondiabetic rats. METHODS: Streptozotocin was used to induce diabetes in half the rats. Two weeks later, the whole corneal epithelium was debrided. Diabetic and healthy rats (3-5 per group) were sacrificed before debridement and 1, 3, and 7 days and 1 month afterwards. The localization of laminin and type IV collagen was observed in cryosections by epifluorescence microscopy. RESULTS: In unwounded corneas of both diabetic and normal rats, laminin and type IV collagen were localized in the corneal epithelial basement. The intensity of fluorescence, however, was clearly stronger in the diabetic rats. In normal rats, wounding initially removed laminin and type IV collagen, but during healing these two proteins reappeared beneath the resurfacing corneal epithelium. Although similar results were observed in diabetic rats, the expression of laminin and type IV collagen was delayed, and their deposition was fragmented and irregular. CONCLUSIONS: These results suggest that delayed corneal epithelial wound healing in diabetes might involve delayed reappearance and abnormal reformation of epithelial basement membrane proteins.
机译:目的:为了了解糖尿病患者角膜基底膜的病理生理,我们比较了糖尿病和非糖尿病大鼠角膜上皮伤口愈合过程中层粘连蛋白和Ⅳ型胶原在上皮基底膜中的定位。方法:链脲佐菌素用于诱导一半的大鼠糖尿病。两周后,清除了整个角膜上皮。在清创前,1、3、7、1个月后,将糖尿病和健康大鼠(每组3-5只)处死。通过落射荧光显微镜在冷冻切片中观察到层粘连蛋白和IV型胶原蛋白的定位。结果:在糖尿病和正常大鼠的未受伤角膜中,层粘连蛋白和IV型胶原均位于角膜上皮基底。然而,糖尿病大鼠的荧光强度明显更强。在正常大鼠中,伤口最初会去除层粘连蛋白和IV型胶原蛋白,但在愈合过程中,这两种蛋白会重新出现在表面角膜上皮细胞下方。尽管在糖尿病大鼠中观察到了相似的结果,但是层粘连蛋白和IV型胶原蛋白的表达被延迟,并且它们的沉积破碎且不规则。结论:这些结果表明,糖尿病患者角膜上皮伤口愈合的延迟可能涉及上皮基底膜蛋白的重新出现和异常重建。

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