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首页> 美国政府科技报告 >Progression of Ocular Sulfur Mustard Injury: Development of a Model System
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Progression of Ocular Sulfur Mustard Injury: Development of a Model System

机译：眼部硫芥伤的进展：模型系统的发展

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Exposure of tissues to sulfur mustard (SM) results in the formation of protein and nucleotide adducts that disrupt cellular metabolism and cause cell death. Subsequent pathologies involve a significant pro inflammatory response, disrupted healing, and long-term defects in tissue architecture. Following ocular exposure, acute corneal sequelae include epithelial erosions, necrosis, and corneal inflammation. Longer term, a progressive injury becomes distributed throughout the anterior chamber, which ultimately causes a profound remodeling of corneal tissues. In many cases, debilitating and vision- threatening injuries reoccur months to years after the initial exposure. Preliminary data in humans suffering from chronic epithelial lesions suggest that thymosin 134 (Ti34) may be a viable candidate to mitigate acute or long- term ocular SM injury. To evaluate therapeutic candidates, we have developed a rabbit ocular exposure model system. In this paper, we report molecular, histological, ultrastructural, and clinical consequences of rabbit ocular SM injury, which can be used to assess Ti34 efficacy, including timepoints at which Ti34 will be assessed for therapeutic utility.

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