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半乳糖血症大鼠的角膜再上皮化

Corneal re-epithelialization in galactosemic rats.

作者信息

Datiles M B, Kador P F, Fukui H N, Hu T S, Kinoshita J H

出版信息

Invest Ophthalmol Vis Sci. 1983 May;24(5):563-9.

PMID:6841002
Abstract

Abnormalities in corneal epithelial healing in diabetic patients have been described recently. Defects in corneal re-epithelialization in diabetic rats have been reported, and it was found that treatment with aldose reductase (AR) inhibitors effectively prevented these defects. Experiments using galactosemic rats to study further the role of AR in these defects, since AR is known to be the common factor involved in sugar cataractogeneses, are reported herein. Similar defects in corneal re-epithelialization in galactosemic rats as in diabetic rats were found. The delay in re-epithelialization was documented by computer planimetry. Light microscopy showed marked corneal stroma edema and wider intercellular spaces in the epithelium after complete re-epithelialization, while scanning electron microscopy revealed fewer filopodia projecting from the leading margin during the active migration stage. These defects were prevented by treating galactosemic rats with the aldose reductase inhibitor, Pfizer's Sorbinil. These suggest that AR plays a role in the defects in corneal re-epithelialization observed in diabetes.

摘要

近期已有关于糖尿病患者角膜上皮愈合异常的描述。有报道称糖尿病大鼠角膜再上皮化存在缺陷,且发现用醛糖还原酶(AR)抑制剂治疗可有效预防这些缺陷。本文报道了使用半乳糖血症大鼠进一步研究AR在这些缺陷中作用的实验,因为AR是已知参与糖性白内障形成的共同因素。发现半乳糖血症大鼠角膜再上皮化存在与糖尿病大鼠类似的缺陷。通过计算机平面测量法记录了再上皮化延迟情况。光镜检查显示完全再上皮化后角膜基质明显水肿且上皮细胞间隙增宽,而扫描电子显微镜显示在活跃迁移阶段前缘伸出的丝状伪足较少。用醛糖还原酶抑制剂辉瑞公司的索比尼尔治疗半乳糖血症大鼠可预防这些缺陷。这些表明AR在糖尿病中观察到的角膜再上皮化缺陷中起作用。

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